Insulin action under arrestin.
Insulin signaling is key to the etiology of metabolic syndrome. Recent work (Luan et al., 2009) uncovers a role for beta-arrestin, previously known to control GPCR desensitization, in insulin signaling. In mouse models, beta-arrestin-2 controls whole-body insulin action by regulating assembly of a complex containing insulin receptor, c-Src, and Akt.
Stöckli
Jacqueline
J
Garvan Institute of Medical Research, 384 Victoria St., Darlinghurst, NSW, Australia.
James
David E
DE
D000818:Animals; D019390:Arrestins / Q000235:genetics / Q000378:metabolism*; D004789:Enzyme Activation; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D024821:Metabolic Syndrome; D051379:Mice; D018345:Mice, Knockout; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D000071560:beta-Arrestin 2; D000071557:beta-Arrestins
C000605254:ARRB2 protein, human; C000605258:Arrb2 protein, mouse; D019390:Arrestins; D007328:Insulin; D000071560:beta-Arrestin 2; D000071557:beta-Arrestins; D051057:Proto-Oncogene Proteins c-akt