Wiley Interdiscip Rev Syst Biol Med - ?-Arrestin-kinase scaffolds: turn them on or turn them off?

Tópicos

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Resumo

G-protein-coupled receptors (GPCRs) can signal through heterotrimeric G-proteins or through ?-arrestins to elicit responses to a plethora of extracellular stimuli. While the mechanisms underlying G-protein signaling is relatively well understood, the mechanisms by which ?-arrestins regulate the diverse set of proteins with which they associate remain unclear. Multi-protein complexes are a common feature of ?-arrestin-dependent signaling. The first two such complexes discovered were the mitogen-activated kinases modules associated with extracellular regulated kinases (ERK1/2) and Jnk3. Subsequently a number of other kinases have been shown to undergo ?-arrestin-dependent regulation, including Akt, phosphatidylinositol-3kinase (PI3K), Lim-domain-containing kinase (LIMK), calcium calmodulin kinase II (CAMKII), and calcium calmodulin kinase kinase ? (CAMKK?). Some are positively and some negatively regulated by ?-arrestin association. One of the missing links to understanding these pathways is the molecular mechanisms by which the activity of these kinases is regulated. Do ?-arrestins merely serve as scaffolds to bring enzyme and substrate together or do they have a direct effect on the enzymatic activities of target kinases? Recent evidence suggests that both mechanisms are involved and that the mechanisms by which ?-arrestins regulate kinase activity varies with the target kinase. This review discusses recent advances in the field focusing on 5 kinases for which considerable mechanistic detail and specific sites of interaction have been elucidated.

Resumo Limpo

gproteincoupl receptor gpcrs can signal heterotrimer gprotein arrestin elicit respons plethora extracellular stimuli mechan under gprotein signal relat well understood mechan arrestin regul divers set protein associ remain unclear multiprotein complex common featur arrestindepend signal first two complex discov mitogenactiv kinas modul associ extracellular regul kinas erk jnk subsequ number kinas shown undergo arrestindepend regul includ akt phosphatidylinositolkinas pik limdomaincontain kinas limk calcium calmodulin kinas ii camkii calcium calmodulin kinas kinas camkk posit negat regul arrestin associ one miss link understand pathway molecular mechan activ kinas regul arrestin mere serv scaffold bring enzym substrat togeth direct effect enzymat activ target kinas recent evid suggest mechan involv mechan arrestin regul kinas activ vari target kinas review discuss recent advanc field focus kinas consider mechanist detail specif site interact elucid

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