Activation of the CRF 1 receptor causes ERK1/2 mediated increase in GRK3 expression in CATH.a cells

G-protein coupled receptor kinase 3 (GRK3) mediates desensitization of alpha 2-adrenergic (α 2-AR) and CRF 1 receptors. CRF 1 receptors, α 2-AR and GRK3, are localized to the primary source of noradrenergic inputs to higher brain centers critical in both the response to stress and the development of...

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Bibliographic Details
Published in:FEBS letters 2007-07, Vol.581 (17), p.3204-3210
Main Authors: Salim, Samina, Hite, Brian, Eikenburg, Douglas C.
Format: Article
Language:English
Subjects:
Bipolar disorder
Kinase
Nucleus
Protein synthesis
Stress
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Summary:G-protein coupled receptor kinase 3 (GRK3) mediates desensitization of alpha 2-adrenergic (α 2-AR) and CRF 1 receptors. CRF 1 receptors, α 2-AR and GRK3, are localized to the primary source of noradrenergic inputs to higher brain centers critical in both the response to stress and the development of depression, namely, locus coeruleus (LC). This study utilizing CATH.a cells (derived from the LC), demonstrates for the first time, that the stress hormone, CRF selectively up-regulates GRK3 expression via an ERK1/2-mediated mechanism accompanied by the activation of Sp-1 and Ap-2 transcription factors. This observation has important implications for the regulation of stress signaling in the brain.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2007.06.006