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J Biol Chem, Vol. 274, Issue 2, 993-999, January 8, 1999

Kalirin Inhibition of Inducible Nitric-oxide Synthase

Edward A. RatovitskiDagger , M. Rashidul Alam§, Richard A. QuickDagger , Audrey McMillanDagger , Clare BaoDagger , Chaim KozlovskyDagger , Tracey A. Hand§, Richard C. Johnson§, Richard E. Mains§, Betty A. Eipper§, and Charles J. LowensteinDagger

From the Division of Cardiology, Dagger  Department of Medicine, and § Department of Neurosciences, School of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Nitric oxide (NO) acts as a neurotransmitter. However, excess NO produced from neuronal NO synthase (nNOS) or inducible NOS (iNOS) during inflammation of the central nervous system can be neurotoxic, disrupting neurotransmitter and hormone production and killing neurons. A screen of a hippocampal cDNA library showed that a unique region of the iNOS protein interacts with Kalirin, previously identified as an interactor with a secretory granule peptide biosynthetic enzyme. Kalirin associates with iNOS in vitro and in vivo and inhibits iNOS activity by preventing the formation of iNOS homodimers. Expression of exogenous Kalirin in pituitary cells dramatically reduces iNOS inhibition of ACTH secretion. Thus Kalirin may play a neuroprotective role during inflammation of the central nervous system by inhibiting iNOS activity.

Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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