Regulation of a novel αN-catenin splice variant in schizophrenic smokers
The αN‐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 αN‐ca...
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Veröffentlicht in: | American journal of medical genetics. Part B, Neuropsychiatric genetics Neuropsychiatric genetics, 2008-09, Vol.147B (6), p.759-768 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | The αN‐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 αN‐catenin splice variant (αN‐catenin III) is described. A comparison of αN‐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 αN‐catenin III as a novel disease susceptibility gene. © 2007 Wiley‐Liss, Inc. |
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ISSN: | 1552-4841 1552-485X |
DOI: | 10.1002/ajmg.b.30679 |