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Regulation of $Ca^{2+}/$ calmodulin kinase II inhibitor \alpha (CaMKIINa) in virus-infected mouse brain

Saha, Sougata and Ramanathan, Anand and Rangarajan, Pundi N (2006) Regulation of $Ca^{2+}/$ calmodulin kinase II inhibitor \alpha (CaMKIINa) in virus-infected mouse brain. In: Biochemical and Biophysical Research Communications, 350 (2). pp. 444-449.

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Abstract

The \alpha and $_\beta$ isoforms of rat $Ca^{2+}/$ calmodulin kinase II inhibitor (CaMKIIN\alpha/$_\beta$) expressed in brain or brain and testis, respectively, are potent inhibitors of $Ca^{2+}/$ calmodulin kinase II (CaMKII) in vitro. However, the regulation or function of CaMKIIN\alpha/$_\beta$ in the central nervous system (CNS) is not known. In this study, we demonstrate that mouse CaMKIIN\alpha gene encodes a 2.9 kb brain-specific transcript whose expression is downregulated in mouse brain during Japanese encephalitis virus (JEV) and rabies virus infection. The downregulation is specific for CaMKIIN\alpha but not CaMKIIN$_\beta$ mRNA. In addition to these changes in CaMKIIN\alpha mRNA, distinct changes are also observed in the phosphorylation as well as subcellular localization of CaMKII\alpha leading to an increase in cytosolic CaMKII activity in JEV-infected mouse brain. The differential regulation of CaMKII\alpha and CaMKIIN\alpha during JEV infection suggests a possible role for these proteins in viral infection and/or virus-induced neuropathogenesis in the CNS.

Item Type: Journal Article
Additional Information: Copyright of this article belongs to Elsevier.
Keywords: Ca2+/calmodulin kinase II;Ca2+/calmodulin kinase II inhibitor;Central nervous system;Japanese encephalitis virus;Postsynaptic density;Rabies virus
Department/Centre: Division of Biological Sciences > Biochemistry
Date Deposited: 23 Nov 2006
Last Modified: 19 Sep 2010 04:32
URI: http://eprints.iisc.ernet.in/id/eprint/8941

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