pubmed-article:17006543 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17006543 | lifeskim:mentions | umls-concept:C0753114 | lld:lifeskim |
pubmed-article:17006543 | lifeskim:mentions | umls-concept:C0812222 | lld:lifeskim |
pubmed-article:17006543 | lifeskim:mentions | umls-concept:C1519751 | lld:lifeskim |
pubmed-article:17006543 | lifeskim:mentions | umls-concept:C0699900 | lld:lifeskim |
pubmed-article:17006543 | lifeskim:mentions | umls-concept:C0243125 | lld:lifeskim |
pubmed-article:17006543 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
pubmed-article:17006543 | pubmed:issue | 20 | lld:pubmed |
pubmed-article:17006543 | pubmed:dateCreated | 2006-10-18 | lld:pubmed |
pubmed-article:17006543 | pubmed:abstractText | G-protein-coupled receptor kinase 2 (GRK2) is a central regulator of G-protein-coupled receptor signaling. We report that Mdm2, an E3-ubiquitin ligase involved in the control of cell growth and apoptosis, plays a key role in GRK2 degradation. Mdm2 and GRK2 association is enhanced by beta(2)-adrenergic receptor stimulation and beta-arrestin. Increased Mdm2 expression accelerates GRK2 proteolysis and promotes kinase ubiquitination at defined residues, whereas GRK2 turnover is markedly impaired in Mdm2-deficient cells. Moreover, we find that activation of the PI3K/Akt pathway by insulin-like growth factor-1 alters Mdm2-mediated GRK2 degradation, leading to enhanced GRK2 stability and increased kinase levels. These data put forward a novel mechanism for controlling GRK2 expression in physiological and pathological conditions. | lld:pubmed |
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pubmed-article:17006543 | pubmed:language | eng | lld:pubmed |
pubmed-article:17006543 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17006543 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17006543 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:17006543 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17006543 | pubmed:month | Oct | lld:pubmed |
pubmed-article:17006543 | pubmed:issn | 0261-4189 | lld:pubmed |
pubmed-article:17006543 | pubmed:author | pubmed-author:PenelaPetroni... | lld:pubmed |
pubmed-article:17006543 | pubmed:author | pubmed-author:MayorFederico... | lld:pubmed |
pubmed-article:17006543 | pubmed:author | pubmed-author:SalcedoAlicia... | lld:pubmed |
pubmed-article:17006543 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17006543 | pubmed:day | 18 | lld:pubmed |
pubmed-article:17006543 | pubmed:volume | 25 | lld:pubmed |
pubmed-article:17006543 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17006543 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17006543 | pubmed:pagination | 4752-62 | lld:pubmed |
pubmed-article:17006543 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:17006543 | pubmed:year | 2006 | lld:pubmed |