CIDeRplusGeneral Information:
| Id: | 5,317 |
| Diseases: |
Diabetes mellitus, type II
- [OMIM]
Insulin resistance |
| Mus musculus | |
| male | |
| BTO:0001169 3T3-F442A cell | |
| article | |
| Reference: | Ye L et al.(2012) TRPV4 is a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis Cell 151: 96-110 [PMID: 23021218] |
Interaction Information:
| Comment | Fully differentiated 3T3-F442A adipocytes were treated with a chemical library of 3,000 drugs and drug-like compounds for 20 hr; mRNA from treated cells was then analyzed to quantify the expression of Pgc1alpha. AM-251, a cannabinoid receptor 1 (CB1) antagonist, was identified as one of the primary hits. AM-251 is a structural analog of a well-known CB1 antagonist, rimonabant, an antiobesity drugthatwas in clinical use in Europe. Although AM-251 is annotated as a CB1 antagonist, two other CB1 antagonists, SLV319 and CAY10508, failed to induce Pgc1alpha at any dose tested. |
|
Formal Description Interaction-ID: 52024 |
|
| Drugbank entries | Show/Hide entries for CNR1 |
| Comment | Fully differentiated 3T3-F442A adipocytes were treated with a chemical library of 3,000 drugs and drug-like compounds for 20 hr; mRNA from treated cells was then analyzed to quantify the expression of Pgc1alpha. AM-251, a cannabinoid receptor 1 (CB1) antagonist, was identified as one of the primary hits. AM-251 is a structural analog of a well-known CB1 antagonist, rimonabant, an antiobesity drugthatwas in clinical use in Europe. Although AM-251 is annotated as a CB1 antagonist, two other CB1 antagonists, SLV319 and CAY10508, failed to induce Pgc1alpha at any dose tested. |
|
Formal Description Interaction-ID: 52219 |
|
| Comment | Fully differentiated 3T3-F442A adipocytes were treated with a chemical library of 3,000 drugs and drug-like compounds for 20 hr; mRNA from treated cells was then analyzed to quantify the expression of Pgc1alpha. AM-251, a cannabinoid receptor 1 (CB1) antagonist, was identified as one of the primary hits. AM-251 is a structural analog of a well-known CB1 antagonist, rimonabant, an antiobesity drugthatwas in clinical use in Europe. Although AM-251 is annotated as a CB1 antagonist, two other CB1 antagonists, SLV319 and CAY10508, failed to induce Pgc1alpha at any dose tested. |
|
Formal Description Interaction-ID: 52220 |
|
| Drugbank entries | Show/Hide entries for CNR1 |
| Comment | Fully differentiated 3T3-F442A adipocytes were treated with a chemical library of 3,000 drugs and drug-like compounds for 20 hr; mRNA from treated cells was then analyzed to quantify the expression of Pgc1alpha. AM-251, a cannabinoid receptor 1 (CB1) antagonist, was identified as one of the primary hits. AM-251 is a structural analog of a well-known CB1 antagonist, rimonabant, an antiobesity drugthatwas in clinical use in Europe. Although AM-251 is annotated as a CB1 antagonist, two other CB1 antagonists, SLV319 and CAY10508, failed to induce Pgc1alpha at any dose tested. |
|
Formal Description Interaction-ID: 52221 |
drug/chemical compound SLV319 NOT affects_expression of gene/protein |
| Comment | Fully differentiated 3T3-F442A adipocytes were treated with a chemical library of 3,000 drugs and drug-like compounds for 20 hr; mRNA from treated cells was then analyzed to quantify the expression of Pgc1alpha. AM-251, a cannabinoid receptor 1 (CB1) antagonist, was identified as one of the primary hits. AM-251 is a structural analog of a well-known CB1 antagonist, rimonabant, an antiobesity drugthatwas in clinical use in Europe. Although AM-251 is annotated as a CB1 antagonist, two other CB1 antagonists, SLV319 and CAY10508, failed to induce Pgc1alpha at any dose tested. |
|
Formal Description Interaction-ID: 52222 |
|
| Drugbank entries | Show/Hide entries for CNR1 |
| Comment | Fully differentiated 3T3-F442A adipocytes were treated with a chemical library of 3,000 drugs and drug-like compounds for 20 hr; mRNA from treated cells was then analyzed to quantify the expression of Pgc1alpha. AM-251, a cannabinoid receptor 1 (CB1) antagonist, was identified as one of the primary hits. AM-251 is a structural analog of a well-known CB1 antagonist, rimonabant, an antiobesity drugthatwas in clinical use in Europe. Although AM-251 is annotated as a CB1 antagonist, two other CB1 antagonists, SLV319 and CAY10508, failed to induce Pgc1alpha at any dose tested. |
|
Formal Description Interaction-ID: 52223 |
drug/chemical compound CAY10508 NOT affects_expression of gene/protein |
| Comment | mRNAs encoding Trpv1, Trpv2, and Trpv4 were expressed in 3T3-F442A adipocytes, with Trpv4 being expressed at the highest level. |
|
Formal Description Interaction-ID: 52224 |
|
| Drugbank entries | Show/Hide entries for TRPV1 |
| Comment | mRNAs encoding Trpv1, Trpv2, and Trpv4 were expressed in 3T3-F442A adipocytes, with Trpv4 being expressed at the highest level. |
|
Formal Description Interaction-ID: 52225 |
|
| Comment | mRNAs encoding Trpv1, Trpv2, and Trpv4 were expressed in 3T3-F442A adipocytes, with Trpv4 being expressed at the highest level. |
|
Formal Description Interaction-ID: 52226 |
|
| Comment | TRPV4 negatively regulated the expression of PGC1alpha. |
|
Formal Description Interaction-ID: 52227 |
|
| Comment | TRPV4 is a calcium-permeable ion channel that was first identified as an osmolality sensor. Since then, many physical and chemical stimuli have been shown to activate TRPV4, including heat, mechanical stress, anandamide, arachidonic acid, and its derivatives. Beta-adrenergic signaling is important for the induction of PGC1alpha and its thermogenic targets; when cells were exposed to norepinephrine, mRNA expression of Pgc1alpha and Ucp1 was robustly increased in the TRPV4 knockdown cells compared to controls. |
|
Formal Description Interaction-ID: 52228 |
drug/chemical compound increases_expression of gene/protein |
| Comment | TRPV4 is a calcium-permeable ion channel that was first identified as an osmolality sensor. Since then, many physical and chemical stimuli have been shown to activate TRPV4, including heat, mechanical stress, anandamide, arachidonic acid, and its derivatives. Beta-adrenergic signaling is important for the induction of PGC1alpha and its thermogenic targets; when cells were exposed to norepinephrine, mRNA expression of Pgc1alpha and Ucp1 was robustly increased in the TRPV4 knockdown cells compared to controls. |
|
Formal Description Interaction-ID: 52229 |
drug/chemical compound increases_expression of gene/protein |
| Comment | TRPV4 is a calcium-permeable ion channel that was first identified as an osmolality sensor. Since then, many physical and chemical stimuli have been shown to activate TRPV4, including heat, mechanical stress, anandamide, arachidonic acid, and its derivatives. Beta-adrenergic signaling is important for the induction of PGC1alpha and its thermogenic targets; when cells were exposed to norepinephrine, mRNA expression of Pgc1alpha and Ucp1 was robustly increased in the TRPV4 knockdown cells compared to controls. |
|
Formal Description Interaction-ID: 52230 |
|
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52231 |
|
| Drugbank entries | Show/Hide entries for CYCS |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52232 |
|
| Drugbank entries | Show/Hide entries for CYCS |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52233 |
|
| Drugbank entries | Show/Hide entries for MT-CO3 |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52234 |
|
| Drugbank entries | Show/Hide entries for MT-CO3 |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52235 |
|
| Drugbank entries | Show/Hide entries for COX4I1 |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52236 |
|
| Drugbank entries | Show/Hide entries for COX4I1 |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52237 |
|
| Drugbank entries | Show/Hide entries for COX5B |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52238 |
|
| Drugbank entries | Show/Hide entries for COX5B |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52239 |
|
| Drugbank entries | Show/Hide entries for COX7A1 |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52240 |
|
| Drugbank entries | Show/Hide entries for COX7A1 |
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52241 |
|
| Comment | PGC1alpha is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cytochrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b. Higher mRNA and protein expression of these genes was observed in TRPV4 knockdown adipocytes. These changes were dependent on the induction of PGC1alpha, as the increased expression of these genes was attenuated by expression of an shRNA against PGC1alpha. |
|
Formal Description Interaction-ID: 52242 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52243 |
|
| Drugbank entries | Show/Hide entries for CCL2 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52244 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52245 |
|
| Drugbank entries | Show/Hide entries for CCL5 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52246 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52247 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52248 |
|
| Drugbank entries | Show/Hide entries for CCL8 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52249 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52250 |
|
| Drugbank entries | Show/Hide entries for CXCL10 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52251 |
|
| Drugbank entries | Show/Hide entries for IL6 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52252 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52253 |
|
| Drugbank entries | Show/Hide entries for THBS1 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52254 |
|
| Drugbank entries | Show/Hide entries for TLR2 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52255 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52256 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52257 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52258 |
|
| Drugbank entries | Show/Hide entries for MMP2 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52259 |
|
| Drugbank entries | Show/Hide entries for FAS |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52260 |
|
| Drugbank entries | Show/Hide entries for VCAM1 |
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52261 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52262 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52263 |
|
| Comment | Knockdown of TRPV4 had a profound inhibitory effect on a whole array of chemokines such as Ccl2 (Mcp1), Ccl3 (Mip1alpha), Ccl5 (Rantes), Ccl7 (Mcp3), Cxcl1 (KC), Ccl8, Cxcl5, and Cxcl10 and cytokines such as Il6, Saa3, and Thrombospondin. A similar effect was observed on the expression of other genes important for inflammatory processes, such as Tlr2, Timp1, Socs3, Socs5, Mmp2, Fas, and Vcam. Conversely, mRNA expression of Mip1alpha, Cxcl1, Il6, Timp1, and Tlr2 can be induced by the TRPV4 agonist. This effect is specific and dependent on TRPV4, as shRNA against TRPV4 fully abolished the induction caused by the agonist. mRNA expression changes for other adipokines, such as Adiponectin, Leptin, RBP4, and Resistin, were also observed. |
|
Formal Description Interaction-ID: 52264 |
|
| Comment | Addition of the TRPV4 agonist to 3T3-F442A adipocytes caused a rapid phosphorylation of both ERK1/2 and JNK1/2 at sites known to reflect activation of these kinases. In contrast, no activating phosphorylation on p38 MAPK was detected with TRPV4 agonism. |
|
Formal Description Interaction-ID: 52265 |
gene/protein increases_activity of gene/protein MAPK3/1 |
| Comment | Addition of the TRPV4 agonist to 3T3-F442A adipocytes caused a rapid phosphorylation of both ERK1/2 and JNK1/2 at sites known to reflect activation of these kinases. In contrast, no activating phosphorylation on p38 MAPK was detected with TRPV4 agonism. |
|
Formal Description Interaction-ID: 52266 |
|
| Comment | Addition of the TRPV4 agonist to 3T3-F442A adipocytes caused a rapid phosphorylation of both ERK1/2 and JNK1/2 at sites known to reflect activation of these kinases. In contrast, no activating phosphorylation on p38 MAPK was detected with TRPV4 agonism. |
|
Formal Description Interaction-ID: 52267 |
|
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52295 |
|
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52296 |
drug/chemical compound GSK205 decreases_activity of |
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52297 |
|
| Drugbank entries | Show/Hide entries for ADRB3 |
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52298 |
|
| Drugbank entries | Show/Hide entries for CYCS |
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52299 |
|
| Drugbank entries | Show/Hide entries for COX7A1 |
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52300 |
drug/chemical compound GSK205 increases_expression of gene/protein |
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52301 |
|
| Drugbank entries | Show/Hide entries for CCL2 |
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52302 |
|
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52303 |
|
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52304 |
|
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52305 |
drug/chemical compound GSK205 increases_activity of process |
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52306 |
drug/chemical compound GSK205 decreases_activity of process |
| Comment | GSK205 potently antagonized TRPV4 in 3T3-F442A adipocytes, as it effectively blocked the calcium influx caused by TRPV4 agonist. Treating these adipocytes with GSK205 for 4 days resulted in increased expression of thermogenic genes and was also accompanied by a decrease in the proinflammatory gene program. This shift resembled the gene expression changes seen in TRPV4-deficient adipocytes. |
|
Formal Description Interaction-ID: 52309 |
gene/protein increases_activity of |