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安全信息

SAB4504503

Sigma-Aldrich

Anti-phospho-p53 (pSer46) antibody produced in rabbit

affinity isolated antibody

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About This Item

UNSPSC代码:
12352203
NACRES:
NA.41

生物来源

rabbit

质量水平

偶联物

unconjugated

抗体形式

affinity isolated antibody

抗体产品类型

primary antibodies

克隆

polyclonal

表单

buffered aqueous solution

分子量

antigen 43 kDa

种属反应性

human, rat, mouse

浓度

~1 mg/mL

技术

ELISA: 1:5000
western blot: 1:500-1:1000

NCBI登记号

UniProt登记号

运输

wet ice

储存温度

−20°C

靶向翻译后修饰

phosphorylation (pSer46)

基因信息

human ... TP53(7157)

免疫原

The antiserum was produced against synthesized peptide derived from human p53 around the phosphorylation site of Ser46.

Immunogen Range: 11-60

特点和优势

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

外形

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

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.

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储存分类代码

10 - Combustible liquids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable

法规信息

新产品

历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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Laiqing Xie et al.
Journal of cellular and molecular medicine, 25(3), 1700-1711 (2021-01-14)
Wet age-related macular degeneration (wAMD), characterized by choroidal neovascularization (CNV), is a leading cause of irreversible vision loss among elderly people in developed nations. Subretinal fibrosis, mediated by epithelial-mesenchymal transition (EMT) of retinal pigment epithelium (RPE) cells, leads to unsuccessful
Pei He et al.
Frontiers in cell and developmental biology, 8, 539485-539485 (2020-10-06)
In zygotes, the capacity of G2/M checkpoint and DNA repair mechanisms to respond to DNA damage varies depending on different external stressors. In our previous studies, we found that mild oxidative stress induced a G2/M phase delay in mouse zygotes

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