General Information:
Id: | 4,033 |
Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance Parkinson disease |
Homo sapiens | |
article | |
Reference: | Gieger C et al.(2008) Genetics meets metabolomics: a genome-wide association study of metabolite profiles in human serum PLoS Genet. 4 [PMID: 19043545] |
Interaction Information:
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41558 |
SNP decreases_activity of gene/protein |
Drugbank entries | Show/Hide entries for FADS1 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41559 |
SNP decreases_quantity of drug/chemical compound PC aa C36:4 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41560 |
SNP decreases_quantity of drug/chemical compound PC a C20:4 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41561 |
SNP decreases_quantity of drug/chemical compound PC aa C38:4 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41562 |
SNP decreases_quantity of drug/chemical compound PC ae C36:5 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41563 |
SNP decreases_quantity of drug/chemical compound SM C22:2 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41564 |
SNP decreases_quantity of drug/chemical compound PC ae C38:4 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41565 |
SNP decreases_quantity of drug/chemical compound PC ae C38:5 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41566 |
SNP decreases_quantity of drug/chemical compound PC aa C38:5 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41567 |
SNP decreases_quantity of drug/chemical compound PC ae C36:4 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41568 |
SNP decreases_quantity of drug/chemical compound PE a C10:0 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41569 |
SNP decreases_quantity of drug/chemical compound SM (COOH) C18:3 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41570 |
SNP decreases_quantity of drug/chemical compound PC aa C34:4 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41571 |
SNP decreases_quantity of drug/chemical compound PC aa C36:5 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41572 |
SNP decreases_quantity of drug/chemical compound PC aa C40:5 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41573 |
SNP decreases_quantity of drug/chemical compound |
Drugbank entries | Show/Hide entries for |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41574 |
SNP decreases_quantity of drug/chemical compound PC ae C40:5 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41575 |
SNP decreases_quantity of drug/chemical compound PC aa C40:4 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41576 |
SNP decreases_quantity of drug/chemical compound SM (OH) C26:1 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41577 |
SNP decreases_quantity of drug/chemical compound SM C24:2 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41578 |
SNP decreases_quantity of drug/chemical compound PI aa C38:4 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41579 |
SNP decreases_quantity of drug/chemical compound SM (OH) C24:0 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41580 |
SNP decreases_quantity of drug/chemical compound PA aa C20:7 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41581 |
SNP decreases_quantity of drug/chemical compound PC ae C38:6 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41583 |
SNP decreases_quantity of drug/chemical compound PC aa C38:6 |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41584 |
SNP decreases_quantity of drug/chemical compound Glytarylcarnitine |
Comment | SNP rs174548, one of several SNPs that lie in a linkage disequilibrium block containing the FADS1 gene was strongly associated with a number of glycerophospholipid concentrations. The FADS1 gene codes for the fatty acid delta-5 desaturase, a key enzyme in the metabolism of long-chain polyunsaturated omega-3 and omega-6 fatty acids. The minor allele variant of this SNP results in a reduced efficiency of the fatty acid delta-5 desaturase reaction, a fact that can be inferred from the following observations: the concentrations of numerous phosphatidylcholines (PC aa C34:4, PC aa C36:4, PC aa C36:5, PC aa C38:4, PC aa C38:5, PC aa C38:6, PC aa C40:4, PC aa C40:5), plasmalogen/plasmenogen phosphatidylcholines (PC ae C36:4, PC ae C38:4, PC ae C38:5, PC ae C38:6, PC ae C40:5), and the phosphatidylinositol PI aa C38:4 with four and more double bonds in their polyunsaturated fatty acid (PUFA) side chains are lowest in individuals that carry the minor allele of rs174548. In particular, the concentrations of the direct product of FADS1, arachidonic acid as well as those of its lyso-phosphatidylcholine derivative (PC a C20:4) are found to be significantly reduced with increasing copy number of the minor allele. |
Formal Description Interaction-ID: 41585 |
SNP decreases_quantity of drug/chemical compound SM C28:4 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41586 |
SNP increases_quantity of drug/chemical compound PE aa C34:2 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41588 |
SNP increases_quantity of drug/chemical compound PE e (COOH) C16:3 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41589 |
SNP increases_quantity of drug/chemical compound PC aa C34:2 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41590 |
SNP increases_quantity of drug/chemical compound PC ae C36:2 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41591 |
SNP increases_quantity of drug/chemical compound PI aa C36:2 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41592 |
SNP increases_quantity of drug/chemical compound PC aa (OH, COOH) C30:4 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41593 |
SNP increases_quantity of drug/chemical compound PC ae C34:2 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41594 |
SNP increases_quantity of drug/chemical compound |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41595 |
SNP increases_quantity of drug/chemical compound PE aa C36:2 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41596 |
SNP increases_quantity of drug/chemical compound PC aa (COOH) C30:3 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41597 |
SNP increases_quantity of drug/chemical compound SM (OH,COOH) C6:0 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41598 |
SNP increases_quantity of drug/chemical compound PI a (OH, COOH) C18:2 |
Comment | Concentrations of glycerophospholipids with three and less double bonds in their PUFA side chains show a positive association with the FADS1 genotype. These metabolites include the phosphatidylcholines PC aa C34:2 and PC aa C36:2, the plasmalogen/plasmenogen phosphatidylcholines PC ae C34:2 and PC ae C36:2, the phosphatidylethanolamines PE aa C34:2 and PE aa C36:2, and the phosphatidylinositol PI aa C36:2. |
Formal Description Interaction-ID: 41599 |
SNP increases_quantity of drug/chemical compound PC aa C36:2 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41611 |
SNP increases_quantity of drug/chemical compound PE aa C38:6 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41614 |
SNP increases_quantity of drug/chemical compound PE aa C40:6 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41615 |
SNP increases_quantity of drug/chemical compound PE aa C38:5 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41616 |
SNP increases_quantity of drug/chemical compound PE aa C36:4 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41617 |
SNP increases_quantity of drug/chemical compound PC aa (COOH) C30:4 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41618 |
SNP increases_quantity of drug/chemical compound PE aa C38:4 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41619 |
SNP increases_quantity of drug/chemical compound PE aa C34:2 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41620 |
SNP increases_quantity of drug/chemical compound PC aa (COOH) C30:3 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41621 |
SNP increases_quantity of drug/chemical compound SM C16:0 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41622 |
SNP increases_quantity of drug/chemical compound PC ae C34:6 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41623 |
SNP increases_quantity of drug/chemical compound PE aa C40:5 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41624 |
SNP decreases_quantity of drug/chemical compound |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41625 |
SNP increases_quantity of drug/chemical compound SM C16:1 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41626 |
SNP increases_quantity of drug/chemical compound SM C28:3 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41627 |
SNP increases_quantity of drug/chemical compound PC aa C38:6 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41628 |
SNP increases_quantity of drug/chemical compound SM (COOH) C16:2 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41629 |
SNP increases_quantity of drug/chemical compound SM C14:0 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41630 |
SNP decreases_quantity of drug/chemical compound Leucine/Isoleucine |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41631 |
SNP increases_quantity of drug/chemical compound SM (OH, COOH) C14:1 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41632 |
SNP increases_quantity of drug/chemical compound PC ae C40:5 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41633 |
SNP increases_quantity of drug/chemical compound PI a (OH) C12:3 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41635 |
SNP increases_quantity of drug/chemical compound PE aa C36:2 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41636 |
SNP decreases_quantity of drug/chemical compound |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41637 |
SNP increases_quantity of drug/chemical compound PC aa (COOH) C30:2 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41638 |
SNP increases_quantity of drug/chemical compound PC ae C38:6 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41639 |
SNP increases_quantity of drug/chemical compound PC ae (OH, COOH) C30:3 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41640 |
SNP increases_quantity of drug/chemical compound PC aa C40:6 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41641 |
SNP increases_quantity of drug/chemical compound PI aa C38:3 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41642 |
SNP increases_quantity of drug/chemical compound PE a (OH, COOH) C12:2 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41643 |
SNP increases_quantity of drug/chemical compound PE e (OH) C18:1 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41644 |
SNP increases_quantity of drug/chemical compound PC aa (COOH) C26:2 |
Comment | SNP rs4775041 is located in a linkage disequilibrium block containing the gene coding for LIPC, a key enzyme of the long-chain fatty acid metabolism. This polymorphism associates with the concentrations of numerous glycerophosphatidylcholines, glycerophosphatidylethanolamines and sphingomyelins. Homozygotes carrying the minor allele have on average 70% higher concentrations of the phosphatidylethanolamine diacyl C38:6 (PE aa C38:6) than homozygotes for the major allele. The molecular function of LIPC is to break-down triglycerides to diacyl- and monoacylglycerols and fatty acids, which makes this association functionally plausible. In previous GWA studies this locus was reported to be associated with HDL cholesterol and triglyceride levels. |
Formal Description Interaction-ID: 41645 |
SNP decreases_quantity of drug/chemical compound |
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41650 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41652 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41653 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41655 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41656 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41657 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41658 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41659 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41660 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41661 |
SNP affects_activity of phenotype abnormal circulating Met.sulf/Glu ratio |
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41662 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41663 |
|
Comment | A polymorphism in the PARK2 gene (rs992037) alters the concentrations of several amino acids. Some of these amino acids are directly connected to the urea cycle. PARK2 codes for parkin, a ubiquitin ligase for which a loss-of-function mutation has been reported to result in Parkinson's disease. When using ratios between metabolite concentrations we observed up to three orders of magnitude smaller p-values. This suggests that this polymorphism impacts some metabolic pathway that involves glutamate on the one hand and a number of other amino acids (except lysine) on the other hand. Thus, the metabolic footprint of this association is that of an amino acid interconversion, which is supported by the functional role of PARK2 as a ubiquitin ligase in the protein degradation pathway. |
Formal Description Interaction-ID: 41664 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41665 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41736 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41737 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41738 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41739 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41740 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41741 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41742 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41743 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41744 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41745 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41746 |
SNP increases_quantity of drug/chemical compound PC aa (OH, COOH) C28:4 |
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41747 |
SNP decreases_quantity of drug/chemical compound PI aa (OH, COOH) C28:2 |
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41748 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41749 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41750 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41751 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41752 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41753 |
SNP increases_quantity of drug/chemical compound PE ae (OH, COOH) C14:2 |
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41754 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41755 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41756 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41757 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41758 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41759 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41760 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41761 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41762 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41763 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41764 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41765 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41766 |
SNP increases_quantity of drug/chemical compound PC ae (OH, COOH) C30:4 |
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41767 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41768 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41769 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41770 |
SNP increases_quantity of drug/chemical compound PC aa (OH, COOH) C30:4 |
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41771 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41772 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41773 |
|
Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41774 |
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Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41775 |
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Comment | SNP rs9309413 lies 21 kb upstream of PLEK. The PLEK gene codes for pleckstrin, a protein that has been proposed to facilitate protein-lipid interactions and to affect membrane structure. SNP rs9309413 impacts on a number of sphingomyelins, which are known to play a major role in membrane lipid structure. |
Formal Description Interaction-ID: 41776 |
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Comment | The study identified two new loci: the first polymorphism is located in the gene coding for the short-chain acyl-Coenzyme A dehydrogenase (SCAD; e.g. intronic SNP rs2014355), the second lies in the gene coding for the mediumchain acyl-Coenzyme A dehydrogenase (MCAD; e.g. intronic SNP rs11161510). Both genes code for enzymes that initiate the beta-oxidation of fatty acids, but they differ in the preference for their chain lengths. The metabolite pair that associates most strongly with rs2014355 of SCAD is the ratio between the shortchain acylcarnitines C3 and C4, while the pair that associates most strongly with rs11161510 of MCAD is the ratio between the medium-chain acylcarnitines C12 and C8. Fatty acids are bound to free carnitine for transport and beta-oxidation into the mitochondria. The short-chain acylcarnitines can be considered as indirect substrates and products of SCAD and the medium-chain acylcarnitines as indirect substrates of MCAD, which matches the biochemical function of these enzymes. From the direction of the effect of these polymorphisms (higher concentrations of the longer chain fatty acids (= substrates) when compared to the smaller chain fatty acids (= products) implies a reduced dehydrogenase activity) it can further be deduced that in both cases minor allele homozygotes have the lowest enzymatic turnover for these reactions. |
Formal Description Interaction-ID: 41777 |
SNP affects_activity of phenotype abnormal circulating acylcarnitine C3/C4 ratio |
Comment | The study identified two new loci: the first polymorphism is located in the gene coding for the short-chain acyl-Coenzyme A dehydrogenase (SCAD; e.g. intronic SNP rs2014355), the second lies in the gene coding for the mediumchain acyl-Coenzyme A dehydrogenase (MCAD; e.g. intronic SNP rs11161510). Both genes code for enzymes that initiate the beta-oxidation of fatty acids, but they differ in the preference for their chain lengths. The metabolite pair that associates most strongly with rs2014355 of SCAD is the ratio between the shortchain acylcarnitines C3 and C4, while the pair that associates most strongly with rs11161510 of MCAD is the ratio between the medium-chain acylcarnitines C12 and C8. Fatty acids are bound to free carnitine for transport and beta-oxidation into the mitochondria. The short-chain acylcarnitines can be considered as indirect substrates and products of SCAD and the medium-chain acylcarnitines as indirect substrates of MCAD, which matches the biochemical function of these enzymes. From the direction of the effect of these polymorphisms (higher concentrations of the longer chain fatty acids (= substrates) when compared to the smaller chain fatty acids (= products) implies a reduced dehydrogenase activity) it can further be deduced that in both cases minor allele homozygotes have the lowest enzymatic turnover for these reactions. |
Formal Description Interaction-ID: 41778 |
SNP affects_activity of phenotype abnormal circulating acylcarnitine C12/C8 ratio |
Comment | The study identified two new loci: the first polymorphism is located in the gene coding for the short-chain acyl-Coenzyme A dehydrogenase (SCAD; e.g. intronic SNP rs2014355), the second lies in the gene coding for the mediumchain acyl-Coenzyme A dehydrogenase (MCAD; e.g. intronic SNP rs11161510). Both genes code for enzymes that initiate the beta-oxidation of fatty acids, but they differ in the preference for their chain lengths. The metabolite pair that associates most strongly with rs2014355 of SCAD is the ratio between the shortchain acylcarnitines C3 and C4, while the pair that associates most strongly with rs11161510 of MCAD is the ratio between the medium-chain acylcarnitines C12 and C8. Fatty acids are bound to free carnitine for transport and beta-oxidation into the mitochondria. The short-chain acylcarnitines can be considered as indirect substrates and products of SCAD and the medium-chain acylcarnitines as indirect substrates of MCAD, which matches the biochemical function of these enzymes. From the direction of the effect of these polymorphisms (higher concentrations of the longer chain fatty acids (= substrates) when compared to the smaller chain fatty acids (= products) implies a reduced dehydrogenase activity) it can further be deduced that in both cases minor allele homozygotes have the lowest enzymatic turnover for these reactions. |
Formal Description Interaction-ID: 41779 |
SNP decreases_activity of gene/protein |
Drugbank entries | Show/Hide entries for ACADS |
Comment | The study identified two new loci: the first polymorphism is located in the gene coding for the short-chain acyl-Coenzyme A dehydrogenase (SCAD; e.g. intronic SNP rs2014355), the second lies in the gene coding for the mediumchain acyl-Coenzyme A dehydrogenase (MCAD; e.g. intronic SNP rs11161510). Both genes code for enzymes that initiate the beta-oxidation of fatty acids, but they differ in the preference for their chain lengths. The metabolite pair that associates most strongly with rs2014355 of SCAD is the ratio between the shortchain acylcarnitines C3 and C4, while the pair that associates most strongly with rs11161510 of MCAD is the ratio between the medium-chain acylcarnitines C12 and C8. Fatty acids are bound to free carnitine for transport and beta-oxidation into the mitochondria. The short-chain acylcarnitines can be considered as indirect substrates and products of SCAD and the medium-chain acylcarnitines as indirect substrates of MCAD, which matches the biochemical function of these enzymes. From the direction of the effect of these polymorphisms (higher concentrations of the longer chain fatty acids (= substrates) when compared to the smaller chain fatty acids (= products) implies a reduced dehydrogenase activity) it can further be deduced that in both cases minor allele homozygotes have the lowest enzymatic turnover for these reactions. |
Formal Description Interaction-ID: 41780 |
SNP decreases_activity of gene/protein |
Drugbank entries | Show/Hide entries for ACADM |