Regulation of Sodium Channel Isoform Expression in Vivo

Rich, Mark M.

Abstract

Funding Agency

• Agency: National Institute of Health (NIH)
• Institute: National Institute of Neurological Disorders and Stroke (NINDS)
• Type: Clinical Investigator Award (CIA) (K08)
• Project #: 1K08NS001852-01
• Application #: 2260064
• Study Section: NST-2 Subcommittee (NST)
• Project Start: 1995-12-08
• Project End: 2000-11-30
• Budget Start: 1995-12-08
• Budget End: 1996-11-30
• Support Year: 1
• Fiscal Year: 1996

Institution

• Name: University of Pennsylvania
• Department: Neurology
• Type: Schools of Medicine
• DUNS #: 042250712
• City: Philadelphia
• State: PA
• Country: United States
• Zip Code: 19104

Publications

Rich, M M; Pinter, M J (2001) Sodium channel inactivation in an animal model of acute quadriplegic myopathy. Ann Neurol 50:26-33

Rich, M M; Kraner, S D; Barchi, R L (1999) Altered gene expression in steroid-treated denervated muscle. Neurobiol Dis 6:515-22

Kraner, S D; Rich, M M; Sholl, M A et al. (1999) Interaction between the skeletal muscle type 1 Na+ channel promoter E-box and an upstream repressor element. Release of repression by myogenin. J Biol Chem 274:8129-36

Kraner, S D; Rich, M M; Kallen, R G et al. (1998) Two E-boxes are the focal point of muscle-specific skeletal muscle type 1 Na+ channel gene expression. J Biol Chem 273:11327-34

Rich, M M; Pinter, M J; Kraner, S D et al. (1998) Loss of electrical excitability in an animal model of acute quadriplegic myopathy. Ann Neurol 43:171-9

Nastuk, M A; Lieth, E; Ma, J Y et al. (1991) The putative agrin receptor binds ligand in a calcium-dependent manner and aggregates during agrin-induced acetylcholine receptor clustering. Neuron 7:807-18