HUMAN GLUR6 KAINATE RECEPTOR (GRIK2) - MOLECULAR-CLONING, EXPRESSION, POLYMORPHISM, AND CHROMOSOMAL ASSIGNMENT

被引:48
作者
PASCHEN, W
BLACKSTONE, CD
HUGANIR, RL
ROSS, CA
机构
[1] JOHNS HOPKINS UNIV,SCH MED,MOLEC NEUROBIOL LAB,BALTIMORE,MD 21205
[2] JOHNS HOPKINS UNIV,SCH MED,PROGRAM MOLEC & CELLULAR BIOL,BALTIMORE,MD 21205
[3] JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205
[4] JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205
[5] MAX PLANCK INST NEUROL RES,DEPT EXPTL NEUROL,COLOGNE,GERMANY
关键词
D O I
10.1006/geno.1994.1198
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
Glutamate receptors mediate the majority of excitatory neurotransmission in the brain, and molecular cloning studies have revealed several distinct families. Because neuropathological states and possibly human disorders may involve kainate-preferring glutamate receptors, we have isolated a cDNA clone for the human GluR6 kainate-preferring receptor. This clone shows a very high sequence similarity with that of the rat, except for a part of the 3' untranslated region in which there is a TAA triplet repeat. When the protein was overexpressed in human embryonic kidney 293 cells, it had a molecular weight, an antibody recognition, and a glutamate ligand-binding profile similar to those of the rat GluR6 receptor. Northern analysis showed expression in both human cerebral and cerebellar cortices. By PCR analysis of rodent-human monochromosomal cell lines, the human GluR6 could be assigned to chromosome 6. The length of the TAA triplet repeat was polymorphic in the normal population, with at least four alleles and an observed heterozygosity of about 45%. These studies should provide the basis for expression or linkage studies of the GluR6 kainate receptor in human disease or neuropathologic states. (C) 1994 Academic Press, Inc.
引用
收藏
页码:435 / 440
页数:6
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