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Annotation

Korostishevsky M, Kremer I, Kaganovich M, Cholostoy A, Murad I, Muhaheed M, Bannoura I, Rietschel M, Dobrusin M, Bening-Abu-Shach U, Belmaker RH, Maier W, Ebstein RP, Navon R. Transmission disequilibrium and haplotype analyses of the G72/G30 locus: Suggestive linkage to schizophrenia in Palestinian Arabs living in the North of Israel. Am J Med Genet B Neuropsychiatr Genet . 2005 Aug 4 ; PubMed Abstract

Comments on Related News
Related News: Genetic Studies of DAOA(G72)/G30 Bridge Kraepelinian Divide

Comment by:  Patricia Estani
Submitted 23 April 2006 Posted 23 April 2006
  I recommend the Primary Papers

Related News: Genetic Studies of DAOA(G72)/G30 Bridge Kraepelinian Divide

Comment by:  Edward Scolnick
Submitted 23 April 2006 Posted 23 April 2006

I would caution that G72 has not been shown to be an actual gene, and in the four years since Chumakov and colleagues' report, the biochemistry has not been reproduced.

View all comments by Edward Scolnick


Related News: Genetic Studies of DAOA(G72)/G30 Bridge Kraepelinian Divide

Comment by:  Nick CraddockMichael Owen (SRF Advisor)
Submitted 26 April 2006 Posted 26 April 2006

Reply to comment by Dr Scolnick
We agree that caution is required regarding the assumption that the genetic association at this locus is causally related to the DAOA "gene," and this is the reason that in the paper we have referred to the "DAOA/ G30 locus." Establishing robust genetic association in a restricted region of the genome is clearly the first step on a path to characterizing the biological and phenotypic relationships associated with the variation. It is entirely possible that pathologically relevant variation occurs at the DAOA/G30 locus that does not involve a protein product of the DAOA DNA sequence.

View all comments by Nick Craddock
View all comments by Michael Owen


Related News: Genetic Studies of DAOA(G72)/G30 Bridge Kraepelinian Divide

Comment by:  Daniel Weinberger, SRF Advisor
Submitted 10 May 2006 Posted 10 May 2006

The DAOA/G30 locus is a paradigm of association in psychiatric genetics, where positive reports are followed by both confirmation of association and failures to associate, with the observers of the glass being half-full commenting that it is unlikely that replication would occur spuriously multiple times, and those seeing the glass as half-empty (or three-quarters empty) emphasizing allelic inconsistencies, lack of identified causative SNPs, and in the case of DAOA/G30, lack of conclusive evidence of a gene expressed in brain. Clearly, we are just scratching the surface of understanding the reasons for any association signal in this region of the genome. It is important to remember that the DAOA/G30 locus was cloned from a region that has shown linkage in a number of studies, giving prior probability to association analyses, and that association has been reported in samples from a number of corners of the world. Expression may be restricted to discrete times in development and may not be present in abundance in middle-aged brains. It is also possible, as noted by Mike Owen,...  Read more


View all comments by Daniel Weinberger
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