| Literature DB >> 18163523 |
Sharon Mexal1, Ralph Berger, Lucy Pearce, Amanda Barton, Judy Logel, Catherine E Adams, Randal G Ross, Robert Freedman, Sherry Leonard.
Abstract
The alphaN-catenin (CTNNA2) gene represents a promising candidate gene for schizophrenia based upon previous genetic linkage, expression, and mouse knockout studies. CTNNA2 is differentially regulated by smoking in schizophrenic patients. In this report, the genomic structure of a primate-specific alphaN-catenin splice variant (alphaN-catenin III) is described. A comparison of alphaN-catenin III mRNA expression across postmortem hippocampi from schizophrenic and non-mentally ill smokers and non-smokers revealed a significant decrease in expression among patient non-smokers compared to all other groups. The recent evolutionary divergence of this gene, as well as the differences in gene expression in postmortem brain of schizophrenic non-smokers, supports the role of alphaN-catenin III as a novel disease susceptibility gene. 2007 Wiley-Liss, Inc.Entities:
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Year: 2008 PMID: 18163523 PMCID: PMC2701353 DOI: 10.1002/ajmg.b.30679
Source DB: PubMed Journal: Am J Med Genet B Neuropsychiatr Genet ISSN: 1552-4841 Impact factor: 3.568