General Information:

Id: 1,310 (click here to show other Interactions for entry)
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
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

in mutant SOD1G85R mice