Activation of the CRF1 receptor causes ERK1/2 mediated increase in GRK3 expression in CATH.a cells

G‐protein coupled receptor kinase 3 (GRK3) mediates desensitization of alpha2‐adrenergic (α2‐AR) and CRF1 receptors. CRF1 receptors, α2‐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 depr...

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Bibliographic Details
Published inFEBS letters Vol. 581; no. 17; pp. 3204 - 3210
Main Authors Salim, Samina, Hite, Brian, Eikenburg, Douglas C.
Format Journal Article
LanguageEnglish
Published 10.07.2007
Subjects
adrenoceptor
Bipolar disorder
EPI
epinephrine
ERK
extracellular signal-regulated kinase
G-protein coupled receptor kinases
G-protein coupled receptors
GPCRs
GRK
Kinase
MAPK
MAPK/ERK kinase
MEK
mitogen-activated protein kinase
Nucleus
polyvinylidene difluoride
Protein synthesis
PVDF
reverse transcriptase polymerase chain reaction
RT-PCR
Stress
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Summary:G‐protein coupled receptor kinase 3 (GRK3) mediates desensitization of alpha2‐adrenergic (α2‐AR) and CRF1 receptors. CRF1 receptors, α2‐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