1p34.3 deletion involvingGRIK3: Further clinical implication of GRIK family glutamate receptors in the pathogenesis of developmental delay-Reference-Cited by-同舟云学术

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1p34.3 deletion involvingGRIK3: Further clinical implication of GRIK family glutamate receptors in the pathogenesis of developmental delay

Published:2013-11-25 Issue:2 Volume:164 Page:456-460
ISSN:1552-4825
Container-title:American Journal of Medical Genetics Part A
language:en
Short-container-title:Am. J. Med. Genet.

Author:

Takenouchi Toshiki¹,Hashida Noriko¹,Torii Chiharu²,Kosaki Rika³,Takahashi Takao¹,Kosaki Kenjiro²

Affiliation:

1. Department of Pediatrics; Keio University School of Medicine; Tokyo Japan

2. Center for Medical Genetics; Keio University School of Medicine; Tokyo Japan

3. Division of Medical Genetics; National Center for Child Health and Development; Tokyo Japan

Publisher

Wiley

Subject

Genetics(clinical),Genetics

Link

http://onlinelibrary.wiley.com/wol1/doi/10.1002/ajmg.a.36240/fullpdf

Reference33 articles.

1. Association between the ionotropic glutamate receptor kainate 3 (GRIK3) ser310ala polymorphism and schizophrenia;Begni;Mol Psychiatry,2002

2. Cloning of a putative glutamate receptor: A low affinity kainate-binding subunit;Bettler;Neuron,1992

3. Missense mutations in COL8A2, the gene encoding the alpha2 chain of type VIII collagen, cause two forms of corneal endothelial dystrophy;Biswas;Hum Mol Genet,2001

4. Detailed phenotype-genotype study in five patients with chromosome 6q16 deletion: Narrowing the critical region for Prader-Willi-like phenotype;Bonaglia;Eur J Hum Genet,2008

5. Kainate receptors are involved in synaptic plasticity;Bortolotto;Nature,1999

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