Chromosomal localization of glutamate receptor genes: Relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans

Paul Gregor; Roger H. Reeves; Ethylin W. Jabs; Xiaodong Yang; William Dackowski; Julie M. Rochelle; Robert H. Brown; Jonathan L. Haines; Bruce F. O'Hara; George R. Uhl; Michael F. Seldin

Chromosomal localization of glutamate receptor genes: Relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans

Paul Gregor, Roger H. Reeves, Ethylin W. Jabs, Xiaodong Yang, William Dackowski, Julie M. Rochelle, Robert H. Brown, Jonathan L. Haines, Bruce F. O'Hara, George R. Uhl, Michael F. Seldin

School of Medicine

Research output: Contribution to journal › Article › peer-review

42 Scopus citations

Abstract

Receptors for the major excitatory neurotransmitter glutamate may play key roles in neurodegeneration. The mouse Glur-5 gene maps to chromosome 16 between App and Sod-1. The homologous human GLUR5 gene maps to the corresponding region of human chromosome 21, which contains the locus for familial amyotrophic lateral sclerosis. This location, and other features, render GLUR5 a possible candidate gene for familial amyotrophic lateral sclerosis. In addition, dosage imbalance of GLUR5 may have a role in the trisomy 21 (Down syndrome). Further characterization of the murine glutamate receptor family includes mapping of Glur-1 to the same region as neurological mutants spasmodic, shaker-2, tipsy, and vibrator on chromosome 11; Glur-2 near spastic on chromosome 3; Glur-6 near waltzer and Jackson circler on chromosome 10; and Glur-7 near clasper on chromosome 4.

Original language	English (US)
Pages (from-to)	3053-3057
Number of pages	5
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	90
Issue number	7
State	Published - Apr 1 1993

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Gregor, P., Reeves, R. H., Jabs, E. W., Yang, X., Dackowski, W., Rochelle, J. M., Brown, R. H., Haines, J. L., O'Hara, B. F., Uhl, G. R., & Seldin, M. F. (1993). Chromosomal localization of glutamate receptor genes: Relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans. Proceedings of the National Academy of Sciences of the United States of America, 90(7), 3053-3057.

Chromosomal localization of glutamate receptor genes: Relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans. / Gregor, Paul; Reeves, Roger H.; Jabs, Ethylin W. et al.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 90, No. 7, 01.04.1993, p. 3053-3057.

Research output: Contribution to journal › Article › peer-review

Gregor, P, Reeves, RH, Jabs, EW, Yang, X, Dackowski, W, Rochelle, JM, Brown, RH, Haines, JL, O'Hara, BF, Uhl, GR & Seldin, MF 1993, 'Chromosomal localization of glutamate receptor genes: Relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans', Proceedings of the National Academy of Sciences of the United States of America, vol. 90, no. 7, pp. 3053-3057.

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abstract = "Receptors for the major excitatory neurotransmitter glutamate may play key roles in neurodegeneration. The mouse Glur-5 gene maps to chromosome 16 between App and Sod-1. The homologous human GLUR5 gene maps to the corresponding region of human chromosome 21, which contains the locus for familial amyotrophic lateral sclerosis. This location, and other features, render GLUR5 a possible candidate gene for familial amyotrophic lateral sclerosis. In addition, dosage imbalance of GLUR5 may have a role in the trisomy 21 (Down syndrome). Further characterization of the murine glutamate receptor family includes mapping of Glur-1 to the same region as neurological mutants spasmodic, shaker-2, tipsy, and vibrator on chromosome 11; Glur-2 near spastic on chromosome 3; Glur-6 near waltzer and Jackson circler on chromosome 10; and Glur-7 near clasper on chromosome 4.",

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Chromosomal localization of glutamate receptor genes: Relationship to familial amyotrophic lateral sclerosis and other neurological disorders of mice and humans

Abstract

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