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Acta Biochimica et Biophysica Sinica Advance Access originally published online on March 8, 2009
Acta Biochimica et Biophysica Sinica 2009 41(4):295-300; doi:10.1093/abbs/gmp013
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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

KChIP1: a potential modulator to GABAergic system

Hui Xiong1,2,{dagger}, Kun Xia3,5,{dagger}, Benshang Li4, Guoping Zhao1 and Zhuohua Zhang2,3,*

1 School of Life Sciences, Fudan University, Shanghai 200433, China
2 Burnham Institute for Medical Research, La Jolla, CA, USA
3 The State Key Lab of Medical Genetics, Institute of Medical Genetics, Central South University, Changsha 410078, China
4 Shanghai Laboratory of Disease and Health Genomics, Chinese National Human Genome Center, Shanghai 201203, China
5 School of Biological Science, Central South University, Changsha 410078, China

* Correspondence address. Tel: +86-731-4805358; Fax: +86-731-4478152; E-mail: benzz{at}burnham.org


  Abstract

Compelling evidences from transgenic mice, immunoprecipitation data, gene expression analysis, and functional heterologous expression studies supported the role of Kv channel interacting proteins (KChIPs) as modulators of Kv4 (Shal) channels underlying the cardiac transient outward current and neuronal A-type current. Till now, there are four members (KChIP1–4) identified in this family. KChIP1 is expressed predominantly in brain, with relative abundance in Purkinje cells of cerebellum, the reticular thalamic nuclei, the medial habenular nuclei, the hippocampus, and striatum. Our results from in situ hybridization and immunostaining assay revealed that KChIP1 was expressed in a subpopulation of parvalbumin-positive neurons suggesting its functional relationship with the GABAergic inhibitory neurons. Moreover, results obtained from KChIP1-deficient mice showed that KChIP1 mutation did not impair survival or alter the overall brain architecture, arguing against its essential function in brain development. However, the mice bearing KChIP1 deletion showed increased susceptibility to anti-GABAergic convulsive drug pentylenetetrazole-induced seizure, indicating that KChIP1 might play pivotal roles in the GABAergic inhibitory system.

Keywords    KChIP; GABA; Kv4; ion channel

Received: November 25, 2008; Accepted: February 16, 2009

{dagger} These authors contributed equally to this work.


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