Glucose homeostasis is regulated by hormones and cellular energy status. Elevations of blood glucose during feeding stimulate insulin release from pancreatic beta-cells through a glucose sensing pathway. Feeding also stimulates the release of gut hormones such as glucogon-like peptide-1 (GLP-1), which induces insulin release, inhibits glucagon release and promotes beta-cell viability. Studies suggest a role for CREB-dependent transcription in glucose sensing and GLP-1 signaling (1). Furthermore, Torc2 (transducer of regulated CREB activity 2), a co-activator of CREB (2,3), is implicated in mediating the effects of these two pathways (4). In quiescent cells, Torc2 is phosphorylated at Ser171 and is consequently sequestered in the cytoplasm via its interaction with 14-3-3 proteins. Glucose and gut hormones lead to the dephosphorylation of Torc2 and its subsequent dissociation with 14-3-3 proteins. Dephosphorylated Torc2 then enters into the nucleus and promotes CREB-dependent transcription. Torc2 is also shown to play a key role in the regulation of hepatic gluconeogenic gene transcription in response to hormonal and energy signals during fasting (5). In addition, two Torc2-related proteins, Torc1 and Torc3, have been identified (2,3). Both Torc1 and Torc3 are also CREB co-activators (3). Torc1, Torc2 and Torc3 have been shown to associate with Tax directly and promote Tax-dependent transcription of human T-cell leukemia virus type I long terminal repeats (6,7).
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