추천 제품
일반 설명
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.
면역원
Linear peptide corresponding to human ATM/ATR (Thr1989).
애플리케이션
Research Category
Epigenetics & Nuclear Function
Epigenetics & Nuclear Function
Research Sub Category
Nuclear Receptors
Nuclear Receptors
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).
품질
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.
표적 설명
~300 kDa observed
물리적 형태
Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
저장 및 안정성
Stable for 1 year at 2-8°C from date of receipt.
면책조항
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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Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
Hyoung Kim et al.
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.
Nam, EA; Zhao, R; Glick, GG; Bansbach, CE; Friedman, DB; Cortez, D
The Journal of Biological Chemistry null
Katarzyna B Leszczynska et al.
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
Yannick P Kok et al.
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
Haineng Xu et al.
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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