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A beta-adrenergic receptor kinase-like enzyme is involved in olfactory signal termination.

Authors: Schleicher, S  Boekhoff, I  Arriza, J  Lefkowitz, RJ  Breer, H 
Citation: Schleicher S, etal., Proc Natl Acad Sci U S A. 1993 Feb 15;90(4):1420-4.
Pubmed: (View Article at PubMed) PMID:8381966

We have previously shown that second-messenger-dependent kinases (cAMP-dependent kinase, protein kinase C) in the olfactory system are essential in terminating second-messenger signaling in response to odorants. We now document that subtype 2 of the beta-adrenergic receptor kinase (beta ARK) is also involved in this process. By using subtype-specific antibodies to beta ARK-1 and beta ARK-2, we show that beta ARK-2 is preferentially expressed in the olfactory epithelium in contrast to findings in most other tissues. Heparin, an inhibitor of beta ARK, as well as anti-beta ARK-2 antibodies, (i) completely prevents the rapid decline of second-messenger signals (desensitization) that follows odorant stimulation and (ii) strongly inhibits odorant-induced phosphorylation of olfactory ciliary proteins. In contrast, beta ARK-1 antibodies are without effect. Inhibitors of protein kinase A and protein kinase C also block odorant-induced desensitization and phosphorylation. These data suggest that a sequential interplay of second-messenger-dependent and receptor-specific kinases is functionally involved in olfactory desensitization.

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CRRD Object Information
CRRD ID: 5685621
Created: 2012-01-12
Species: All species
Last Modified: 2012-01-12
Status: ACTIVE



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