Article

Regulation of a novel alphaN-catenin splice variant in schizophrenic smokers.

Institute for Behavioral Genetics, Boulder, Colorado, USA.
American Journal of Medical Genetics Part B Neuropsychiatric Genetics (impact factor: 3.7). 01/2008; 147B(6):759-68. DOI:10.1002/ajmg.b.30679 pp.759-68
Source: PubMed

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.

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Keywords

alphaN-catenin
 
alphaN-catenin III
 
alphaN-catenin III mRNA expression
 
gene expression
 
genomic structure
 
non-mentally ill smokers
 
non-smokers
 
novel disease susceptibility gene
 
patient non-smokers
 
previous genetic linkage
 
primate-specific alphaN-catenin splice variant
 
promising candidate gene
 
recent evolutionary divergence
 
schizophrenia
 
schizophrenic non-smokers
 
schizophrenic patients
 
significant decrease