Glucose / Energy Metabolism
| CSTコード |
包装 |
希望納入価格 (円) |
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| #3826S | 100 μL | 46,000 | |
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Torc2抗体製品一覧
3826 の推奨プロトコール
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推奨プロトコールはCST社内試験の徹底的なバリデーションに基づいて作成されておりますので、正確かつ再現性の高い結果が得られます。
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3826:
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Western Blotting
| 用途(希釈倍率) | |
| ウエスタンブロッティング(1:1,000) |
| 特異性・感度 | |
| 内在性レベルのTorc2 タンパク質を検出します。 |
| 使用抗原 | |
| ヒトのTorc2 タンパク質由来の配列(合成ペプチド) |
Western Blotting

Western blot analysis of extracts from 293T cells, using Torc2 Antibody.
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 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, 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 (5). Torc2-related proteins Torc1 and Torc3 also act as CREB co-activators (2,3). Torc1, Torc2 and Torc3 associate with the HTLV Tax protein to promote Tax-dependent transcription of HTLV-1 long terminal repeats (6,7). 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, Torc1 is dephosphorylated and translocates into the nucleus (8). Torc1 is essential for energy balance and fertility (8).
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Hinke, S.A. et al. (2004) J. Physiol. 558, 369-380.
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Conkright, M.D. et al. (2003) Mol. Cell 12, 413-423.
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Iourgenko, V. et al. (2003) Proc. Natl. Acad. Sci. USA 100, 12147-12152.
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Screaton, R.A. et al. (2004) Cell 119, 61-74.
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Koo, S.H. et al. (2005) Nature 437, 1109-1111.
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Koga, H. et al. (2004) J. Biol. Chem. 279, 52978-52983.
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Siu, Y.T. et al. (2006) J. Virol. 80, 7052-7059.
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Altarejos, J.Y. et al. (2008) Nat Med 14, 1112-7.