P/Q-type voltage gated calcium channels and spinocerebellar ataxia type 6
Undergraduate Institution and Major/Degree:
State University of New York at Geneseo
My current research focuses on voltage-dependent calcium channels (VDCCs) and their role in the pathogenesis of spinocerebellar ataxia type six (SCA6). SCA6 is a dominantly inherited progressive ataxia, which leads to marked cerebellar atrophy and specifically Purkinje cell degeneration. SCA6 is caused by a mutation in the CACNA1A gene, which encodes the pore forming subunit (a1A) of the P/Q-type voltage gated calcium channel. We are currently exploring how the SCA6 mutation alters normal functioning of the a1A subunit and how this mutation can cause cell death as observed in SCA6.
- Christopher Gomez
- Paul Mermelstein
- Stanley Thayer
Courses Taken Beyond the Core Courses:
- GCD 8213 Topics in Molecular Biology
- GCD 8151 Advanced Cell Biology
- BIOC 4332 Signal Transduction/Gene Expression
- BIOC 4331 Structure/Catalyst/Metabolism
Graduate Level Minor:
- Society for Neuroscience Annual Meeting - Fall 1999, 2000, 2001, 2002,
- Annual Cell Biology Meeting - Fall 2003
- Paul Mermelstein - Chair
- Harry Orr
- Paul Letourneau
- Christopher Gomez - Advisor
- Boulware MI, Kordasiewicz H, Mermelstein PG. Caveolin proteins are essential for distinct effects of membrane estrogen receptors in neurons. J Neurosci. 2007 Sep 12;27(37):9941-50.
- Raike RS, Kordasiewicz HB, Thompson RM, Gomez CM. Dominant-negative suppression of Cav2.1 currents by alpha(1)2.1 truncations requires the conserved interaction domain for beta subunits. Mol Cell Neurosci. 2007 Feb;34(2):168-77.
- Kordasiewicz HB , Thompson RM, Clark HB, Gomez CM. C-termini of P/Q-type Ca2+ channel alpha1A subunits translocate to nuclei and promote polyglutamine-mediated toxicity. Hum Mol Genet. 2006 May 15;15(10):1587-99.
- North Tonawanda, NY