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

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Schleicher, S; Boekhoff, I; Arriza, J; Lefkowitz, RJ; Breer, H

Published Date

  • February 15, 1993

Published In

Volume / Issue

  • 90 / 4

Start / End Page

  • 1420 - 1424

PubMed ID

  • 8381966

Pubmed Central ID

  • PMC45885

International Standard Serial Number (ISSN)

  • 0027-8424

Digital Object Identifier (DOI)

  • 10.1073/pnas.90.4.1420


  • eng

Conference Location

  • United States