This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Mutations in superoxide dismutase 1 (SOD1) cause familial amyotrophic lateral sclerosis (ALS). Expression of mutant SOD1 (SOD1G93A) in rats causes an ALS-like phenotype. Mutant SOD1 associates with mitochondria from the spinal cord, but not the liver. The proteins that mediate the interaction of SOD1 with mitochondria are unknown. We have immunoprecipitated SOD1 from spinal cord mitochondrial fractions and propose to identify proteins associated with SOD1 by mass spectrometry.
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