Analysis of polyglutamine-coding repeats in the TATA-binding protein in different human populations and in patients with schizophrenia an bipolar affective disorder
Journal Article
·
· American Journal of Medical Genetics
DOI:https://doi.org/10.1002/(SICI)1096-8628(19960920)67:5<495::AID-AJMG12>3.0.CO;2-I·
OSTI ID:539233
- Addenbrooke`s National Health Service Trust, Cambridge (United Kingdom)
- Cambridge Univ. (United Kingdom); and others
A new class of disease (including Huntington disease, Kennedy disease, and spinocerebellar ataxias types 1 and 3) results from abnormal expansions of CAG trinucleotides in the coding regions of genes. In all of these diseases the CAG repeats are thought to be translated into polyglutamine tracts. There is accumulating evidence arguing for CAG trinucleotide expansions as one of the causative disease mutations in schizophrenia and bipolar affective disorder. We and others believe that the TATA-binding protein (TBP) is an important candidate to investigate in these diseases as it contains a highly polymorphic stretch of glutamine codons, which are close to the threshold length where the polyglutamine tracts start to be associated with disease. Thus, we examined the lengths of this polyglutamine repeat in normal unrelated East Anglians, South African Blacks, sub-Saharan Africans mainly from Nigeria, and Asian Indians. We also examined 43 bipolar affective disorder patients and 65 schizophrenic patients. The range of polyglutamine tract-lengths that we found in humans was from 26-42 codons. No patients with bipolar affective disorder and schizophrenia had abnormal expansions at this locus. 22 refs., 1 tab.
- OSTI ID:
- 539233
- Journal Information:
- American Journal of Medical Genetics, Journal Name: American Journal of Medical Genetics Journal Issue: 5 Vol. 67; ISSN 0148-7299; ISSN AJMGDA
- Country of Publication:
- United States
- Language:
- English
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