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No evidence for expanded polyglutamine sequences in bipolar disorder and schizophrenia

Jones, Lesley, Middle, F., Guy, Carol, Spurlock, G., Cairns, N. J., McGuffin, P., Craddock, Nicholas John, Owen, Michael John and O'Donovan, Michael Conlon 1997. No evidence for expanded polyglutamine sequences in bipolar disorder and schizophrenia. Molecular Psychiatry 2 (6) , pp. 478-482. 10.1038/sj.mp.4000297

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Abstract

Several recent studies have suggested that expanded CAG repeats may contribute to the genetic transmission of bipolar disorder and schizophrenia. In all known disorders associated with expanded CAG repeats, the repeat sequence is translated into glutamine. Therefore the simplest hypothesis is that one or more proteins with expanded polyglutamine sequences are involved in the pathogenesis of bipolar disorder and schizophrenia. In order to examine this hypothesis, we have used an antibody against expanded polyglutamine sequences to examine Western blots prepared from lymphoblastoid cell lines of patients with schizophrenia and bipolar disorder. We also examined Western blots prepared from left frontal cortex tissue samples obtained from 11 schizophrenics post mortem. With the exception of the TATA-binding protein (TBP), we did not detect any proteins containing expanded polyglutamine sequences. Our data therefore suggest either that the expanded repeats which are associated with these disorders do not encode polyglutamine, or that they are within genes that are not expressed within the tissues investigated here.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: R Medicine > R Medicine (General)
R Medicine > RZ Other systems of medicine
Publisher: Nature Publishing Group
ISSN: 1359-4184
Last Modified: 17 Apr 2019 20:54
URI: http://orca-mwe.cf.ac.uk/id/eprint/63353

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