Cell Signaling Technology

Product Pathways - DNA Damage

Phospho-53BP1 (Ser1778) Antibody #2675

p53-binding protein 1   P531   p53bp1   TP53BP1   TRP53BP1   Tumor suppressor p53-binding protein 1  

No. Size Price
2675S 100 µl ( 10 western blots ) ¥3,900.00 现货查询 购买询价
2675 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Monkey, Endogenous 450 Rabbit
F 1:100
IF-IC 1:100

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, F=Flow Cytometry, IF-IC=Immunofluorescence (Immunocytochemistry),

Specificity / Sensitivity

Phospho-53BP1 (Ser1778) Antibody detects endogenous levels of 53BP1 only when phosphorylated at serine 1778. Phospho-53BP1 (Ser1778)抗体检测内源性丝氨酸(1778位)被磷酸化的53BP1蛋白。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser1778 of human 53BP1. Antibodies are purified by protein A and peptide affinity chromatography. 该多克隆抗体由合成的人源的针对53BP1蛋白丝氨酸(1778位)磷酸化肽段免疫动物,利用A蛋白和多肽亲和层析的方法纯化获得。

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of HeLa cells, untreated (blue) or UV-treated (green), using Phospho-53BP1 (Ser1778) Antibody compared with a nonspecific negative control antibody (red). 流式细胞方法检测未处理和紫外处理的Hela细胞。蓝色为未处理组,绿色为紫外处理组,红色为非特异结合的阴性对照。使用的抗体为Phospho-53BP1(Ser1778) Antibody。

Western Blotting

Western Blotting

Western blot analysis of extracts from 293 cells, untreated or UV-treated (50 mJ for 2 hours), using Phospho-53BP1 (Ser1778) Antibody (upper) or 53BP1 Antibody #4937 (lower). Western blot方法检测细胞提取物:未处理和紫外处理(50mJ,2小时)的293细胞。使用的抗体为Phospho-53BP1(1778) Antibody(上图)和53BP1 Antibody#4937(下图)。



Confocal immunofluorescent analysis of HeLa cells, untreated (left) or UV-treated (right), using Phospho-53BP1 (Ser1778) Antibody (green). Actin filaments have been labeled with Alexa Fluor® 555 phalloidin (red). 激光共聚焦荧光法检测未处理(左图)和紫外处理(右图)的Hela细胞,使用的抗体为Phospho-53BP1 (Ser1778) Antibody (绿色)。肌动蛋白纤维采用Alexa Fluor® 555 鬼笔环肽(红色)标记。


p53-binding protein 1 (53BP1) was originally identified as a p53 binding partner that could enhance the transcriptional activity of p53 (1,2). 53BP1 consists of two BRCA1 carboxy terminal (BRCT) domains that allow for binding to p53 and a separate domain responsible for binding to phosphorylated histone H2A.X (3). 53BP1 rapidly translocates to nuclear foci following treatment of cells with ionizing radiation (IR) or radiomimetic agents that cause DNA double strand breaks (DSBs) (4,5). Because of this localization to DSBs and homology to the yeast protein Rad9, a role for 53BP1 in DSB repair has been proposed. Recruitment of 53BP1 to sites of DNA damage has been demonstrated to be independent of ATM, NBS1, and DNA-PK (4) and retention of 53BP1 at DNA breaks requires phosphorylated H2A.X (6). In cells lacking 53BP1, phosphorylation of ATM substrates is reduced, suggesting that 53BP1 is upstream of ATM (7). In response to IR, phosphorylation of 53BP1 at serines 6, 25, 29, and 784 by ATM has been demonstrated, but phosphorylation at these sites is not required for localization of 53BP1 to sites of DSBs (6). p53结合蛋白1(p53 binding protein 1,53BPl)最初被认为是一种p53的结合蛋白,其功能是增强p53基因的转录活性。53BP1通过其两个BRCA1羧基末端(BRCT)结构域与p53基因结合,通过另外一个独立的结构域与磷酸化组蛋白H2A.X结合。电离辐射(IR)或者辐射类物预处理细胞后,可引起DNA双链断裂(DSBs),53BP1蛋白迅速转移到核内。鉴于DNA断裂后53BP1的定位改变及其与酵母蛋白Rad9的同源性,人们提出53BP1可能在DNA双链断裂后的修复过程中起到一定的作用。53BP1聚集到DNA损伤处的过程不依赖于ATM,NBS1,和DNA-PK,但是其在DNA断裂处的滞留依赖于磷酸化H2A.X。在53BP1表达缺失的细胞中,ATM底物的磷酸化程度降低,提示53BP1在ATM上游起作用。电离刺激后,53BP1在丝氨酸6,25,29以及784位被ATM磷酸化,但是这些位点的磷酸化并不影响53BP1在DNA双链断裂处的聚集。

Within the first BRCT domain (amino acids 1714-1850), there exists a consensus ATM/ATR phosphorylation site, Ser1778. It is conceivable that phosphorylation of Ser1778 could therefore serve to regulate 53BP1-p53 binding. 第一个BRCT结构域(1714-1850氨基酸)含有一个共同识别ATM/ATR的磷酸化位点:Ser1778。该位点的磷酸化可能调节53BP1-p53 的结合。

  1. Iwabuchi, K. et al. (1994) Proc. Natl. Acad. Sci. USA 91, 6098-6102.
  2. Iwabuchi, K. et al. (1998) J. Biol. Chem. 273, 26061-26068.
  3. Mochan, T.A. et al. (2004) DNA Repair (Amst) 3, 945-952.
  4. Schultz, L.B. et al. (2000) J. Cell Biol. 151, 1381-1390.
  5. Anderson, L. et al. (2001) Mol. Cell. Biol. 21, 1719-1729.
  6. Ward, I.M. et al. (2003) J. Biol. Chem. 278, 19579-19582.
  7. DiTullio, R.A. et al. (2002) Nat. Cell Biol. 4, 998-1002.
  8. Dephoure, N. et al. (2008) Proc Natl Acad Sci U S A 105, 10762-7.

Application References

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