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Proceedings of the National Academy of Sciences - PNAS, 1993-02, Vol.90 (4), p.1420-1424
1993
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Details

Autor(en) / Beteiligte
Titel
A β-Adrenergic Receptor Kinase-Like Enzyme is Involved in Olfactory Signal Termination
Ist Teil von
  • Proceedings of the National Academy of Sciences - PNAS, 1993-02, Vol.90 (4), p.1420-1424
Ort / Verlag
United States: National Academy of Sciences of the United States of America
Erscheinungsjahr
1993
Quelle
MEDLINE
Beschreibungen/Notizen
  • 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 β-adrenergic receptor kinase (βARK) is also involved in this process. By using subtype-specific antibodies to βARK-1 and βARK-2, we show that βARK-2 is preferentially expressed in the olfactory epithelium in contrast to findings in most other tissues. Heparin, an inhibitor of β ARK, as well as anti-βARK-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, βARK-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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