MAPPING OF THE HUMAN NMDA RECEPTOR SUBUNIT (NMDAR1) AND THE PROPOSED NMDA RECEPTOR GLUTAMATE-BINDING SUBUNIT (NMDARA1) TO CHROMOSOME-9Q34.3 AND CHROMOSOME-8, RESPECTIVELY

被引:15
作者
COLLINS, C
DUFF, C
DUNCAN, AMV
PLANELLSCASES, R
SUN, W
NORREMOLLE, A
MICHAELIS, E
MONTAL, M
WORTON, R
HAYDEN, MR
机构
[1] UNIV BRITISH COLUMBIA,DEPT MED GENET,416-2125 EAST MALL,VANCOUVER V6T 2C1,BC,CANADA
[2] HOSP SICK CHILDREN,DEPT GENET,LONDON WC1N 3JH,ENGLAND
[3] UNIV CALIF SAN DIEGO,DEPT BIOL,LA JOLLA,CA 92093
[4] KINGSTON GEN HOSP,DEPT CYTOGENET,KINGSTON K7L 2V7,ONTARIO,CANADA
[5] QUEENS UNIV,KINGSTON K7L 3N6,ONTARIO,CANADA
[6] UNIV KANSAS,DEPT PHARMACOL & TOXICOL,LAWRENCE,KS 66045
关键词
D O I
10.1006/geno.1993.1311
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
A role for the N-methyl-d-aspartate (NMDA) receptor in the molecular pathology underlying Huntington disease (HD) has been proposed on the basis of neurochemical studies in HD and the ability of the NMDA receptor to mediate neuronal cell death. The molecular cloning of the human NMDA receptor subunit (NMDAR1) and a proposed glutamate-binding subunit of the NMDA receptor (NMDARA1) have provided an opportunity to test the hypothesis that either of these genes might be directly involved in the causation of HD. We have mapped NMDAR1 to 9q34.3 using in situ hybridization studies and NMDARA1 to human chromosome 8 using a somatic cell hybrid panel. Because the gene causing HD has been localized to chromosome 4p16.3, the chromosome assignments reported here are inconsistent with either of these genes playing a causative role in the molecular pathology of HD. However, it is noteworthy that the gene for torsion dystonia has also been localized by genetic studies to 9q34.3, the same regional map location as NMDAR1. © 1993 by Academic Press, Inc.
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收藏
页码:237 / 239
页数:3
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