2577 Phospho-Histone H2A.X (Ser139) Antibody #2577

"上海博耀生物销售Phospho-Histone H2A.X (Ser139) Antibody #2577，CST原装品质，价格优惠，订购Phospho-Histone H2A.X (Ser139

"上海博耀生物销售Phospho-Histone H2A.X (Ser139) Antibody #2577，CST原装品质，价格优惠，订购Phospho-Histone H2A.X (Ser139) Antibody #2577，详情请咨询销售人员！
产品详细参数如下>>>>

产品名称：Phospho-Histone H2A.X (Ser139) Antibody #2577
货号：2577
品牌：CST(cell signaling)
抗体来源：Rabbit
克隆类型： Antibodies
规格：

No.	Size	Price
2577S	100 ul (10 western blots)	询价
2577L	300 ul (30 western blots)	询价

抗体应用：

Applications	Reactivity	Sensitivity	MW (kDa)	Source
W IHC-P IF-IC F	H M R	Endogenous	15	Rabbit

Applications Key:  W=Western Blotting  IHC-P=Immunohistochemistry (Paraffin)  IF-IC=Immunofluorescence (Immunocytochemistry)  F=Flow Cytometry
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on sequence homology.
特异性/敏感度： Phospho-H2A.X (Ser139) Antibody detects endogenous levels of H2A.X only when phosphorylated at Ser139.
来源及纯化方法： Antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser139 of human H2A.X.
抗体背景：

Histone H2A.X is a variant histone that represents approximately 10% of the total H2A histone proteins in normal human fibroblasts (1). H2A.X is required for checkpoint-mediated cell cycle arrest and DNA repair following double-stranded DNA breaks (1). DNA damage, caused by ionizing radiation, UV-light, or radiomimetic agents, results in rapid phosphorylation of H2A.X at Ser139 by PI3K-like kinases, including ATM, ATR, and DNA-PK (2,3). Within minutes following DNA damage, H2A.X is phosphorylated at Ser139 at sites of DNA damage (4). This very early event in the DNA-damage response is required for recruitment of a multitude of DNA-damage response proteins, including MDC1, NBS1, RAD50, MRE11, 53BP1, and BRCA1 (1). In addition to its role in DNA-damage repair, H2A.X is required for DNA fragmentation during apoptosis and is phosphorylated by various kinases in response to apoptotic signals. H2A.X is phosphorylated at Ser139 by DNA-PK in response to cell death receptor activation, c-Jun N-terminal Kinase (JNK1) in response to UV-A irradiation, and p38 MAPK in response to serum starvation (5-8). H2A.X is constitutively phosphorylated on Tyr142 in undamaged cells by WSTF (Williams-Beuren syndrome transcription factor) (9,10). Upon DNA damage, and concurrent with phosphorylation of Ser139, Tyr142 is dephosphorylated at sites of DNA damage by recruited EYA1 and EYA3 phosphatases (9). While phosphorylation at Ser139 facilitates the recruitment of DNA repair proteins and apoptotic proteins to sites of DNA damage, phosphorylation at Tyr142 appears to determine which set of proteins are recruited. Phosphorylation of H2A.X at Tyr142 inhibits the recruitment of DNA repair proteins and promotes binding of pro-apoptotic factors such as JNK1 (9). Mouse embryonic fibroblasts expressing only mutant H2A.X Y142F, which favors recruitment of DNA repair proteins over apoptotic proteins, show a reduced apoptotic response to ionizing radiation (9). Thus, it appears that the balance of H2A.X Tyr142 phosphorylation and dephosphorylation provides a switch mechanism to determine cell fate after DNA damage.

关键词：CST，抗体，一抗{byao_back}{byao_back2}

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