CIDeRplusGeneral Information:
| Id: | 1,310 |
| Diseases: |
Amyotrophic lateral sclerosis
|
| Mus musculus | |
| Embryonic motoneurons isolated from E12.5 wild-type mice or mice overexpressing the G85R mutant form of SOD1 (SOD1G85R) | |
| BTO:0000312 motoneuron | |
| article | |
| Reference: | Duplan L et al.(2010) Collapsin response mediator protein 4a (CRMP4a) is upregulated in motoneurons of mutant SOD1 mice and can trigger motoneuron axonal degeneration and cell death J. Neurosci. 30: 785-796 [PMID: 20071543] |
Interaction Information:
| Comment | Proteomic analysis of SOD1G85R motoneurons exposed to nitric oxide revealed increased levels of CRMP4 (DPYSL3) expression. By the treatment of mutant SOD1G85R motoneurons with concentrations of NO (nitric oxide) that are sufficient to trigger mSOD1 motoneuron death but not that of wild-type motoneurons, only CRMP4 (isoform CRMP4a), of all the proteins that can be detected at this level of sensitivity, appeared to be upregulated in a manner that correlated with neuronal susceptibility. |
|
Formal Description Interaction-ID: 8947 |
drug/chemical compound increases_activity of phenotype |
| Comment | Proteomic analysis and immunostainig of SOD1G85R motoneurons exposed to nitric oxide revealed increased levels of CRMP4 (DPYSL3) expression. By the treatment of mutant SOD1G85R motoneurons with concentrations of NO (nitric oxide) that are sufficient to trigger mSOD1 motoneuron death but not that of wild-type motoneurons, only CRMP4 (isoform CRMP4a), of all the proteins that can be detected at this level of sensitivity, appeared to be upregulated in a manner that correlated with neuronal susceptibility. |
|
Formal Description Interaction-ID: 8950 |
|
| Comment | Immunostaining showed that exposure to NO (nitric oxide) in vitro induced an increase in CRMP4a, but not CRMP2 (DPYSL2), in mutant SOD1 motoneurons, but not controls. |
|
Formal Description Interaction-ID: 8951 |
|
| Comment | Overexpression of CRMP4a (DPYSL3, isoform a) led to a 60% reduction in axonal length in motoneurons in contrast to overexpression of CRMP2 which had no significant effect on axonal outgrowth. |
|
Formal Description Interaction-ID: 8955 |
mRNA/protein variant decreases_activity of process |
| Comment | Overexpression of CRMP4a (DPYSL3, isoform a) led to a 60% reduction in axonal length in motoneurons in contrast to overexpression of CRMP2 which had no significant effect on axonal outgrowth. |
|
Formal Description Interaction-ID: 8958 |
gene/protein NOT decreases_activity of process |
| Comment | In marked contrast to the results with motoneurons, neither CRMP4a (DPYSL3, isoform a) nor CRMP2 affected neurite outgrowth from hippocampal neurons. |
|
Formal Description Interaction-ID: 8959 |
mRNA/protein variant NOT affects_activity of process |
| Comment | In marked contrast to the results with motoneurons, neither CRMP4a (DPYSL3, isoform a) nor CRMP2 affected neurite outgrowth from hippocampal neurons. |
|
Formal Description Interaction-ID: 8960 |
gene/protein NOT affects_activity of process |
| Comment | Expression of CRMP4a (DPYSL3, isoform a), but not CRMP2, in cultured embryonic motoneurons was sufficient to trigger a neurodegenerative process involving reduction in axon length and cell death. |
|
Formal Description Interaction-ID: 8961 |
mRNA/protein variant increases_activity of phenotype |
| Comment | Expression of CRMP4a (DPYSL3, isoform a), but not CRMP2, in cultured embryonic motoneurons was sufficient to trigger a neurodegenerative process involving reduction in axon length and cell death. |
|
Formal Description Interaction-ID: 8962 |
gene/protein NOT increases_activity of phenotype |