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

First Author  Salim S Year  2007
Journal  FEBS Lett Volume  581
Issue  17 Pages  3204-10
PubMed ID  17583697 Mgi Jnum  J:123732
Mgi Id  MGI:3719340 Doi  10.1016/j.febslet.2007.06.006
Citation  Salim S, et al. (2007) Activation of the CRF(1) receptor causes ERK1/2 mediated increase in GRK3 expression in CATH.a cells. FEBS Lett 581(17):3204-10
abstractText  G-protein coupled receptor kinase 3 (GRK3) mediates desensitization of alpha(2)-adrenergic (alpha(2)-AR) and CRF(1) receptors. CRF(1) receptors, alpha(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.
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