DNA Damage
Chk1 (2G1D5) Mouse mAb
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| CSTコード |
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希望納入価格 (円) |
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| #2360S | 100 μL | 46,000 | |
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Chk1抗体製品一覧
2360 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。
注:各製品に最適化されたプロトコールをリンクしています。
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2360:
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Western Blotting
| 用途(希釈倍率) | |
| ウェ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Chk1 タンパク質を検出します。 |
Western Blotting

Western blot analysis of extracts from various cell lines using Chk1 (2G1D5) Mouse mAb.
Western Blotting

Western blot analysis of extracts from HeLa cells, transfected with 100 nM SignalSilence® Control siRNA (Fluorescein Conjugate) #6201 (-) or SignalSilence® Chk1 siRNA I #6241 or SignalSilence® Chk1 siRNA II (+), using Chk1 (2G1D5) Mouse mAb #2360 and β-Actin (13E5) Rabbit mAb #4970. Chk1 (2G1D5) Mouse mAb confirms silencing of Chk1 expression and β-Actin (13E5) Rabbit mAb is used to control for loading and specificity of Chk1 siRNA.
Chk1 kinase acts downstream of ATM/ATR kinase and plays an important role in DNA damage checkpoint control, embryonic development, and tumor suppression (1). Activation of Chk1 involves phosphorylation at Ser317 and Ser345 and occurs in response to blocked DNA replication and certain forms of genotoxic stress (2). While phosphorylation at Ser345 serves to localize Chk1 to the nucleus following checkpoint activation (3), phosphorylation at Ser317 along with site-specific phosphorylation of PTEN allows for reentry into the cell cycle following stalled DNA replication (4). Chk1 exerts its checkpoint mechanism on the cell cycle, in part, by regulating the cdc25 family of phosphatases. Chk1 phosphorylation of cdc25A targets it for proteolysis and inhibits its activity through 14-3-3 binding (5). Activated Chk1 can inactivate cdc25C via phosphorylation at Ser216, blocking the activation of cdc2 and transition into mitosis (6). Centrosomal Chk1 has been shown to phosphorylate cdc25B and inhibit its activation of CDK1-cyclin B1, thereby abrogating mitotic spindle formation and chromatin condensation (7). Furthermore, Chk1 plays a role in spindle checkpoint function through regulation of Aurora B and BubR1 (8). Chk1 has emerged as a drug target for cancer therapy as its inhibition leads to cell death in many cancer cell lines (9).
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Liu, Q. et al. (2000) Genes Dev 14, 1448-59.
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Zhao, H. and Piwnica-Worms, H. (2001) Mol Cell Biol 21, 4129-39.
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Jiang, K. et al. (2003) J Biol Chem 278, 25207-17.
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Martin, S.A. and Ouchi, T. (2008) Mol Cancer Ther 7, 2509-16.
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Chen, M.S. et al. (2003) Mol Cell Biol 23, 7488-97.
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Zeng, Y. et al. (1998) Nature 395, 507-10.
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Löffler, H. et al. (2006) Cell Cycle 5, 2543-7.
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Zachos, G. et al. (2007) Dev Cell 12, 247-60.
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Garber, K. (2005) J Natl Cancer Inst 97, 1026-8.