Cell Signaling Technology

Product Pathways - DNA Damage

Phospho-p53 (Thr81) Antibody #2676

Cellular tumor antigen p53   Phosphoprotein p53   pjnk   TP53   Tumor suppressor p53  

No. Size Price
2676S 100 µl ( 10 western blots ) ¥4,050.00 现货查询 购买询价 防伪查询
2676T 20 µl ( 2 western blots ) ¥1,500.00 现货查询 购买询价 防伪查询
2676 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Monkey, Endogenous 53 Rabbit
IHC-P 1:150

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IHC-P=Immunohistochemistry (Paraffin),

Specificity / Sensitivity

Phospho-p53 (Thr81) Antibody detects endogenous levels of p53 only when phosphorylated at threonine 81.Phospho-p53 (Thr81) Antibody 能够检测内源性苏氨酸(81位)磷酸化的p53蛋白。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Thr81 of human p53. Antibodies are purified by protein A and peptide affinity chromatography. 该多克隆抗体是由合成的人源的针对p53蛋白苏氨酸(81位)的磷酸化肽段免疫动物,采用蛋白A和多肽亲和层析技术纯化生产的。



Immunofluorescent analysis of COS-7 cells, untreated (left) or nocodazole-treated (right), using Phospho-p53 (Thr81) Antibody (green) and p53 (1C12) Mouse mAb #2524 (red).免疫荧光方法检测COS-7细胞,未处理组(左图)或诺考达唑处理组(右图),使用的抗体为 Phospho-p53 (Thr81) Antibody,呈绿色,和p53 (1C12) Mouse mAb #2524 ,呈红色。

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded HT-29 cells, untreated (left) or nocodazole-treated (right), using Phospho-p53 (Thr81) Antibody in the presence of control peptide (lower) or antigen-specific peptide (upper). 免疫组织化学方法检测石蜡包埋HT-29细胞,分为非处理组(左图)和诺考达唑处理组(右图),使用的抗体为 Phospho-p53 (Thr81) Antibody ,下图为对照多肽共孵育,上图为抗原特异性多肽共孵育。

Western Blotting

Western Blotting

Western blot analysis of extracts from HT29 cells, untreated, nocodazole-treated (50 ng/ml, 24h) or UV-treated (50mJ/cm2, 1hr), using Phospho-p53 (Thr81) Antibody (upper), p53 (1C12) Mouse mAb #2524 (middle), or Phospho-SAPK/JNK(T183/Y185) (98F2) Rabbit mAb #4671 (lower).Western blot方法检测HT29细胞提取物,分为非处理组、诺考达唑(50 ng/ml) 处理24小时组和紫外处理(50mJ/cm2)1小时组,使用的抗体为Phospho-p53 (Thr81) Antibody (上图), p53 (1C12) Mouse mAb #2524 (中图), 和Phospho-SAPK/JNK(T183/Y185) (98F2) Rabbit mAb #4671 (下图).


The p53 tumor suppressor protein plays a major role in cellular response to DNA damage and other genomic aberrations. Activation of p53 can lead to either cell cycle arrest and DNA repair or apoptosis (1). p53 is phosphorylated at multiple sites in vivo and by several different protein kinases in vitro (2,3). DNA damage induces phosphorylation of p53 at Ser15 and Ser20 and leads to a reduced interaction between p53 and its negative regulator, the oncoprotein MDM2 (4). MDM2 inhibits p53 accumulation by targeting it for ubiquitination and proteasomal degradation (5,6). p53 can be phosphorylated by ATM, ATR, and DNA-PK at Ser15 and Ser37. Phosphorylation impairs the ability of MDM2 to bind p53, promoting both the accumulation and activation of p53 in response to DNA damage (4,7). Chk2 and Chk1 can phosphorylate p53 at Ser20, enhancing its tetramerization, stability, and activity (8,9). p53 is phosphorylated at Ser392 in vivo (10,11) and by CAK in vitro (11). Phosphorylation of p53 at Ser392 is increased in human tumors (12) and has been reported to influence the growth suppressor function, DNA binding, and transcriptional activation of p53 (10,13,14). p53 is phosphorylated at Ser6 and Ser9 by CK1δ and CK1ε both in vitro and in vivo (13,15). Phosphorylation of p53 at Ser46 regulates the ability of p53 to induce apoptosis (16). Acetylation of p53 is mediated by p300 and CBP acetyltransferases. Inhibition of deacetylation suppressing MDM2 from recruiting HDAC1 complex by p19 (ARF) stabilizes p53. Acetylation appears to play a positive role in the accumulation of p53 protein in stress response (17). Following DNA damage, human p53 becomes acetylated at Lys382 (Lys379 in mouse) in vivo to enhance p53-DNA binding (18). Deacetylation of p53 occurs through interaction with the SIRT1 protein, a deacetylase that may be involved in cellular aging and the DNA damage response (19). p53肿瘤抑制蛋白在细胞响应DNA损伤和其它基因组异常的过程中发挥重要作用。p53的激活能够引起细胞周期捕获和DNA修复或细胞凋亡(1)。离体或者在体情况下,p53可以在多个位点被几个蛋白激酶进行磷酸化(2,3)。DNA损伤能够诱导p53的第15位和20位丝氨酸磷酸化,导致p53和其负调节子-癌蛋白MDM2的相互作用减弱(4)。MDM2通过靶向p53促进其泛素化和蛋白酶体降解抑制其累积。P53的第15位和37位丝氨酸可以被ATM,ATR,和DNA-PK磷酸化(5,6)。P53的磷酸化削弱了MDM2的结合,从而促进了它的激活和累积以响应DNA损伤(4,7)。Chk2和Chk1能够磷酸化p53的第20位丝氨酸,增强其四聚化、稳定性和活性(8,9)。p53的第392位丝氨酸可以发生在体磷酸化(10,11)和CAK介导的离体磷酸化(11)。人类肿瘤中p53的第392位丝氨酸磷酸化增加(12)且有报道认为该过程能够影响生长抑制剂的功能、DNA结合和p53的转录激活(10,13,14)。P53的第6位和9位丝氨酸离体或者在体均可以被CK1δ和CK1ε磷酸化(13,15)。P53的第46位丝氨酸磷酸化能够调节p53诱导细胞凋亡的能力(16)。p300和CBP乙酰转移酶能够介导p53的乙酰化。去乙酰化抑制可以阻止MDM2招募p19 (ARF)介导的HDAC1复合体从而稳定p53。乙酰化似乎对于应激反应中p53蛋白的累积起着正向的作用(17)。DNA损伤后,人类p53的第382位赖氨酸(在小鼠为379位赖氨酸)发生在体乙酰化,促进p53-DNA的结合(18)。P53通过与SIRT1蛋白(一种参与细胞衰老和DNA损伤应激的去乙酰酶)相互作用发生去乙酰化(19)。

DNA damage and stress-inducing agents can also result in SAPK/JNK-mediated phosphorylation of p53 at Thr81, and a Thr81Ala mutant p53 does not permit SAPK/JNK-dependent p53 transcriptional activation and apoptosis (17). DNA损伤和应激诱导剂能够引起SAPK/JNK介导的p53第81位苏氨酸磷酸化,而Thr81Ala突变的p53不允许SAPK/JNK依赖的p53转录激活和细胞凋亡(17)。

  1. Levine, A.J. (1997) Cell 88, 323-31.
  2. Meek, D.W. (1994) Semin Cancer Biol 5, 203-10.
  3. Milczarek, G.J. et al. (1997) Life Sci 60, 1-11.
  4. Shieh, S.Y. et al. (1997) Cell 91, 325-34.
  5. Chehab, N.H. et al. (1999) Proc Natl Acad Sci U S A 96, 13777-82.
  6. Honda, R. et al. (1997) FEBS Lett 420, 25-7.
  7. Tibbetts, R.S. et al. (1999) Genes Dev 13, 152-7.
  8. Shieh, S.Y. et al. (1999) EMBO J 18, 1815-23.
  9. Hirao, A. et al. (2000) Science 287, 1824-7.
  10. Hao, M. et al. (1996) J Biol Chem 271, 29380-5.
  11. Lu, H. et al. (1997) Mol Cell Biol 17, 5923-34.
  12. Ullrich, S.J. et al. (1993) Proc Natl Acad Sci U S A 90, 5954-8.
  13. Kohn, K.W. (1999) Mol Biol Cell 10, 2703-34.
  14. Lohrum, M. and Scheidtmann, K.H. (1996) Oncogene 13, 2527-39.
  15. Knippschild, U. et al. (1997) Oncogene 15, 1727-36.
  16. Oda, K. et al. (2000) Cell 102, 849-62.
  17. Ito, A. et al. (2001) EMBO J 20, 1331-40.
  18. Sakaguchi, K. et al. (1998) Genes Dev 12, 2831-41.
  19. Solomon, J.M. et al. (2006) Mol Cell Biol 26, 28-38.
  20. Buschmann, T. et al. (2001) Mol. Cell. Biol. 21, 2743-2754.

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