TORC1/CRTC1 (C71D11) Rabbit mAbProduct information
|100 µl (10 western blots)||-||Unavailable in your region|
Product Pathways - Metabolism
TORC1/CRTC1 (C71D11) Rabbit mAb #2587
|2587S||100 µl (10 western blots)||---||In Stock||---|
|2587||carrier free and custom formulation / quantity||email request|
|W||1:1000||Mouse, Rat||Endogenous||78||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting
Species predicted to react based on 100% sequence homology: Human.
Specificity / Sensitivity
TORC1/CRTC1 (C71D11) Rabbit mAb recognizes endogenous levels of total TORC1 (CRTC1) protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val463 of human TORC1 (CRTC1) protein.
Glucose homeostasis is regulated by hormones and cellular energy status. Elevations of blood glucose during feeding stimulate insulin release from pancreatic β-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 β-cell viability. CREB-dependent transcription likely plays a role in both glucose sensing and GLP-1 signaling (1). The protein CRTC2 (CREB-regulated transcription coactivator 2)/TORC2 (transducer of regulated CREB activity 2) functions as a CREB co-activator (2,3) and is implicated in mediating the effects of these two pathways (4). In quiescent cells, CRTC2/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 CRTC2/TORC2 and its dissociation from 14-3-3 proteins. Dephosphorylated CRTC2/TORC2 enters the nucleus to promote CREB-dependent transcription. CRTC2/TORC2 plays a key role in the regulation of hepatic gluconeogenic gene transcription in response to hormonal and energy signals during fasting (5).
CRTC2/TORC2-related proteins CRTC1/TORC1 and CRTC3/TORC3 also act as CREB co-activators (2,3). CRTC1/TORC1, CRTC2/TORC2 and CRTC3/TORC3 associate with the HTLV Tax protein to promote Tax-dependent transcription of HTLV-1 long terminal repeats (6,7). CRTC1/TORC1 is highly phosphorylated at Ser151 in mouse hypothalamic cells under basal conditions (8). When these cells are exposed to cAMP or a calcium activator, CRTC1/TORC1 is dephosphorylated and translocates into the nucleus (8). CRTC1/TORC1 is essential for energy balance and fertility (8).
- Hinke, S.A. et al. (2004) J Physiol 558, 369-80.
- Conkright, M.D. et al. (2003) Mol Cell 12, 413-23.
- Iourgenko, V. et al. (2003) Proc Natl Acad Sci U S A 100, 12147-52.
- Screaton, R.A. et al. (2004) Cell 119, 61-74.
- Koo, S.H. et al. (2005) Nature 437, 1109-11.
- Koga, H. et al. (2004) J Biol Chem 279, 52978-83.
- Siu, Y.T. et al. (2006) J Virol 80, 7052-9.
- Altarejos, J.Y. et al. (2008) Nat Med 14, 1112-7.
- Jeong, H. et al. (2011) Nat Med 18, 159-65. Applications: Western Blotting.
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U.S. Patent No. 7,429,487, foreign equivalents, and child patents deriving therefrom.