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Activation of the CRF 1 receptor causes ERK1/2 mediated increase in GRK3 expression in CATH.a cells
Author(s) -
Salim Samina,
Hite Brian,
Eikenburg Douglas C.
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.06.006
Subject(s) - locus coeruleus , receptor , adrenergic receptor , desensitization (medicine) , microbiology and biotechnology , endocrinology , chemistry , medicine , hormone , alpha (finance) , signal transduction , kinase , biology , nucleus , biochemistry , construct validity , nursing , patient satisfaction
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.