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詳細
The Ataxia-Telangiectasia and Rad3 related kinase (ATR) is a nuclear serine/threonine kinase that is part of the "first-response" system to DNA damage induced by a wide variety of factors including double-stranded breaks and replication stress. The localization of ATR to sites of DNA damage is aided by the Replication Protein A (RPA). Phospho - ATR (Ser428) targets a number of proteins including BRCA1, WRN, CHEK1, MCM2, and p53/TP53, and coordinates signaling pathways involved in DNA repair and apoptosis. ATR may also be involved in the phosphorylation of the histone H2A.X after replication stress, an early marker of DNA damage. However, ATR also mediates DNA replication and fork stability in normal cell cycles by activation of Chk1. Defective ATR contributes to Seckel syndrome type 1.
免疫原
Linear peptide corresponding to human ATM/ATR (Thr1989).
アプリケーション
Research Category
エピジェネティクス及び核内機能分子
エピジェネティクス及び核内機能分子
Research Sub Category
核受容体
核受容体
This Anti-phospho ATM/ATR (Thr1989) Antibody is validated for use in Western Blotting for the detection of phospho ATM/ATR (Thr1989).
Western Blotting Analysis: A representative lot detected ATM/ATR (Thr1989) in ATR TR cells (Nam, E.A, et al. (2011). JBC. 286(33):28707–28714).
品質
Evaluated by Western Blotting in 2mM hydroxyurea treated 293T cell lysate.
Western Blotting Analysis: 1.0 µg/mL of this antibody detected ATM/ATR (Thr1989) in 10 µg of 2mM hydroxyurea treated 293T cell lysate.
Western Blotting Analysis: 1.0 µg/mL of this antibody detected ATM/ATR (Thr1989) in 10 µg of 2mM hydroxyurea treated 293T cell lysate.
ターゲットの説明
~300 kDa observed
物理的形状
Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
保管および安定性
Stable for 1 year at 2-8°C from date of receipt.
免責事項
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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保管分類コード
12 - Non Combustible Liquids
WGK
WGK 1
引火点(°F)
Not applicable
引火点(℃)
Not applicable
適用法令
試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。
Jan Code
ABE462:
試験成績書(COA)
製品のロット番号・バッチ番号を入力して、試験成績書(COA) を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。
Clinical cancer research : an official journal of the American Association for Cancer Research, 23(12), 3097-3108 (2016-12-21)
Purpose: PARP inhibition (PARPi) has modest clinical activity in recurrent BRCA-mutant (BRCAMUT) high-grade serous ovarian cancers (HGSOC). We hypothesized that PARPi increases dependence on ATR/CHK1 such that combination PARPi with ATR/CHK1 blockade results in increased cell death and tumor regression.Experimental
Thr-1989 phosphorylation is a marker of active ataxia telangiectasia-mutated and Rad3-related (ATR) kinase.
The Journal of Biological Chemistry null
Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology, 121(2), 232-238 (2016-11-15)
Esophageal cancer has a persistently low 5-year survival rate and has recently been classified as a cancer of unmet need by Cancer Research UK. Consequently, new approaches to therapy are urgently required. Here, we tested the hypothesis that an ATR
Oncogenesis, 9(10), 88-88 (2020-10-09)
Oncogene-induced replication stress, for instance as a result of Cyclin E1 overexpression, causes genomic instability and has been linked to tumorigenesis. To survive high levels of replication stress, tumors depend on pathways to deal with these DNA lesions, which represent
Cell reports. Medicine, 2(9), 100394-100394 (2021-10-09)
CCNE1-amplified ovarian cancers (OVCAs) and endometrial cancers (EMCAs) are associated with platinum resistance and poor survival, representing a clinically unmet need. We hypothesized that dysregulated cell-cycle progression promoted by CCNE1 overexpression would lead to increased sensitivity to low-dose WEE1 inhibition
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