General Information:

Id: 310 (click here to show other Interactions for entry)
Diseases: Amyotrophic lateral sclerosis
Mus musculus
SOD1 wt or SOD1G93A or SOD1G85R transgenic mouse, transfected with human wt SOD1 or human SOD1G93A or human SOD1G85R
BTO:0000312 motoneuron
article
Reference: Raoul C et al.(2006) Chronic activation in presymptomatic amyotrophic lateral sclerosis (ALS) mice of a feedback loop involving Fas, Daxx, and FasL Proc. Natl. Acad. Sci. U.S.A. 103: 6007-6012 [PMID: 16581901]

Interaction Information:

Comment In both control and mutant SOD1 motoneurons, exogenous NO (addition of Detanonoate) leads to up-regulation of FasL. As a reporter of Fas activation, phophorylation of p38 kinase was quantified. However, only in the presence of G93A or G85R mutant forms of SOD1 does this mechanism lead to a Fas-dependent increase in phosphorylation of p38 kinase.
Formal Description
Interaction-ID: 1224

drug/chemical compound

NO

increases_quantity of

gene/protein

FASLG

in wt and mutant mice