2595 Histone H2A.X Antibody #2595

"上海博耀生物销售Histone H2A.X Antibody #2595，CST原装品质，价格优惠，订购Histone H2A.X Antibody #2595，详情请咨询销售人

"上海博耀生物销售Histone H2A.X Antibody #2595，CST原装品质，价格优惠，订购Histone H2A.X Antibody #2595，详情请咨询销售人员！
产品详细参数如下>>>>

产品名称：Histone H2A.X Antibody #2595
货号：2595
品牌：CST(cell signaling)
抗体来源：Rabbit
克隆类型： Polyclonal
规格：

No.	Size	Price
2595S	100 ul (10 western blots)	询价

抗体应用：

Applications	Reactivity	Sensitivity	MW (kDa)	Source
W	H M R Mk	Endogenous	15	Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Mon key
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： Histone H2A.X Antibody detects endogenous levels of histone H2A.X protein independent of phosphorylation and ubiquitination.
来源及纯化方法： Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy-terminus of human histone H2A.X. Antibodies are purified by protein A and peptide affinity chromatography.
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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