Merck

P7874

Sigma-Aldrich

Anti- p53 抗体,小鼠单克隆

clone DO-2, purified from hybridoma cell culture

NACRES:
NA.41

生物来源

mouse

质量水平

偶联物

unconjugated

抗体形式

purified from hybridoma cell culture

antibody product type

primary antibodies

克隆

DO-2, monoclonal

形式

buffered aqueous solution

分子量

antigen ~53 kDa

species reactivity

human

浓度

~2 mg/mL

technique(s)

immunoprecipitation (IP): suitable
western blot: 1-2 μg/mL using total cell extract of A431 cells

同位素/亚型

IgG1

UniProt登记号

运输

dry ice

储存温度

−20°C

Gene Information

human ... TP53(7157)

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此商品
P6749P6874P9249
conjugate

unconjugated

conjugate

unconjugated

conjugate

unconjugated

conjugate

biotin conjugate

antibody form

purified from hybridoma cell culture

antibody form

purified immunoglobulin

antibody form

purified immunoglobulin

antibody form

ascites fluid

clone

DO-2, monoclonal

clone

PAb1801, monoclonal

clone

DO-1, monoclonal

clone

DO-1, monoclonal

form

buffered aqueous solution

form

buffered aqueous solution

form

buffered aqueous solution

form

buffered aqueous solution

mol wt

antigen ~53 kDa

mol wt

antigen ~53 kDa

mol wt

antigen ~53 kDa

mol wt

antigen ~53 kDa

一般描述

Monoclonal Anti-p53 (mouse IgG1 isotype) is derived from the hybridoma DO-2 produced by the fusion of mouse myeloma cells (SP2 cells) and splenocytes from BALB/c mice immunized with recombinant human wild type p53.
p53 is a tumor suppressor gene expressed in a wide variety of tissues. It is a tetrameric nuclear DNA-binding phosphoprotein. The gene encoding it is localized on human chromosome 17p13.1 and mouse chromosome 11.

免疫原

recombinant human wild type p53. The antibody epitope resides between amino acids 10-16 of human p53.

应用

Monoclonal Anti-p53-Biotin antibody produced in mouse has been used for DNase I footprint, immunoprecipitation and western blotting.

生化/生理作用

Tumor suppressor p53 has the capability to induce cell cycle arrest and has a role in DNA repair, senescence and apoptosis. It binds to Simian vacuolating virus 40 (SV40) T-antigen and human papilloma virus E6 protein. The p53 gene is mutated in various cancers, such as of the breast, ovarian, bladder, colon and lung.
p53 is phosphorylated at multiple sites by several protein kinases in response to DNA damage. It is essential for the maintenance of the non-tumorigenic phenotype of cells. Phosphorylation of p53 at Ser15 by ataxia telangiectasia mutate (ATM), ataxia telangiectasia and Rad3-related protein (ATR), and DNA-dependent protein kinase (DNA-PK) leads to a reduced interaction with its negative regulator MDM2 and accumulation of p53 protein. Checkpoint kinase 2 (Chk2) and Chk1 can phosphorylate p53 at Ser20, which enhances its activity, tetramerization, and stability. Elevation of p53 protein induces the transcriptional activation of multiple genes, including cyclin-dependent kinase inhibitor 1 (p21waf1).

外形

0.01M 磷酸缓冲盐溶液,pH 7.4,含 15mM 叠氮化钠。

免责声明

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.

储存分类代码

10 - Combustible liquids

WGK

WGK 3

闪点(F)

Not applicable

闪点(C)

Not applicable

个人防护装备

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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p53 C-terminal phosphorylation by CHK1 and CHK2 participates in the regulation of DNA-damage-induced C-terminal acetylation
Ou YH, et al.
Molecular Biology of the Cell, 16(4), 1684-1695 (2005)
Cell Cycle and Apoptosis
Bruna Pucci
Neoplasia, 2(4) (2000)
Augmentation of Radiation-Induced Apoptosis by ellagic acid
Sushma M
Cancer Investigation, 2, 323?330-323?330 (2010)
ATM mediates phosphorylation at multiple p53 sites, including Ser46, in response to ionizing radiation
Saito S, et al.
The Journal of biological chemistry, 277(15), 12491-12494 (2002)
Cell Cycle and Apoptosis
Bruna Pucci
Neoplasia, 2(4) (2000)

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