Kalirin inhibition of inducible nitric-oxide synthase

Edward A. Ratovitski, M. Rashidul Alam, Richard A. Quick, Audrey McMillan, Clare Bao, Chaim Kozlovsky, Tracey A. Hand, Richard C. Johnson, Richard E. Mains, Betty A. Eipper, Charles J. Lowenstein

Research output: Contribution to journalArticlepeer-review

Abstract

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 vive 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.

Original languageEnglish (US)
Pages (from-to)993-999
Number of pages7
JournalJournal of Biological Chemistry
Volume274
Issue number2
DOIs
StatePublished - Jan 8 1999

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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