CRTC2 (CREB-regulated transcription coactivator 2, Torc2) is a CREB coactivator, regulating glucose homeaostatis. Glucose homeostasis is regulated by hormones and cellular energy status. Elevations of blood glucose during feeding stimulate insulin release from pancreatic (B)-cells through a glucose sensing pathway. Feeding also stimulates release of gut hormones such as glucagon-like peptide-1 (GLP-1), which further induces insulin release, inhibits glucagon release and promotes (B)-cell viability. CREB-dependent transcription likely plays a role in both glucose sensing and GLP-1 signaling. Torc2 is implicated in mediating the effects of these two pathways. In quiescent cells, Torc2 is phosphorylated at Ser171 and becomes sequestered in the cytoplasm via an interaction with 14-3-3 proteins. Glucose and gut hormones lead to the dephosphorylation of Torc2 and its dissociation from 14-3-3 proteins. Dephosphorylated Torc2 enters the nucleus to promote CREB-dependent transcription. Torc2 plays a key role in the regulation of hepatic gluconeogenic gene transcription in response to hormonal and energy signals during fasting.Torc2 is most abundantly e, Xenopus/Amphibian,pressed in the thymus. Present in both B and T lymphocytes. Highly e, Xenopus/Amphibian,pressed in HEK293T cells and in insulinomas. High levels also in spleen, ovary,Mouse,uscle and lung, with highest levels in muscle. Lower levels found in brain, colon, heart, kidney,Porcinerostate, small intestine and stomach. Weak e, Xenopus/Amphibian,pression in liver and pancreas.
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