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主要文件

安全信息

A1106

Sigma-Aldrich

抗-ATM抗体,小鼠单克隆

clone MAT3-4G10/8, purified from hybridoma cell culture

别名:

抗共济失调毛细血管扩张突变

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About This Item

MDL编号:
UNSPSC代码:
12352203
NACRES:
NA.45

价格与库存信息目前不能提供

生物来源

mouse

质量水平

重组

expressed in mouse cell line

偶联物

unconjugated

抗体形式

purified from hybridoma cell culture

抗体产品类型

primary antibodies

克隆

MAT3-4G10/8, monoclonal

表单

PBS solution

分子量

antigen ~300 kDa

种属反应性

human, mouse

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706247062371404M
technique(s)

microbiological culture: suitable

technique(s)

microbiological culture: suitable

technique(s)

microbiological culture: suitable

technique(s)

microbiological culture: suitable

growth mode

adherent or suspension

growth mode

adherent or suspension

growth mode

adherent or suspension

growth mode

adherent or suspension

morphology

rod shaped

morphology

rod shaped

morphology

rod shaped

morphology

rod shaped

storage temp.

−70°C

storage temp.

−70°C

storage temp.

−70°C

storage temp.

−70°C

shipped in

dry ice

shipped in

dry ice

shipped in

dry ice, wet ice

shipped in

dry ice

一般描述

单克隆抗ATM(小鼠IgG1同种型)源自通过小鼠骨髓瘤细胞(NSO)融合产生的杂交瘤MAT3-4G10/8和用肽免疫的BALB/c小鼠脾细胞。

特异性

单克隆抗ATM抗体与小鼠和人ATM发生特异性反应。

免疫原

跨越小鼠ATM的1967-1988位的肽,在其NH2末端含有与KLH偶联的半胱氨酸。

应用

ATM单克隆抗体可用于免疫印迹、ELISA和免疫沉淀。

生化/生理作用

抗共济失调毛细血管扩张突变(ATM)负责响应双链断裂(DSB)激活和稳定p53。ATM直接在Ser15上磷酸化p53,并同时激活其他激酶,这些激酶在其他位点磷酸化同一分子。此外,双分钟2(Hdm2)的人类同源物在Ser395上被ATM磷酸化,这种磷酸化抑制了Hdm2介导的p53降解。

外形

0.01 M磷酸盐缓冲液(pH 7.4,含有15 mM叠氮化钠)中的溶液

免责声明

除非我们的产品目录或产品附带的其他公司文档另有说明,否则我们的产品仅供研究使用,不得用于任何其他目的,包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。

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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

常规特殊物品

  • 历史批次信息供参考:

    分析证书(COA)

    Lot/Batch Number

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    访问文档库

    ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage
    Maya R, et al.
    Genes & Development, 15(9), 1067-1067 (2001)
    Jasmin Roohi et al.
    Journal of human genetics, 62(5), 581-584 (2017-01-27)
    Ataxia-telangiectasia (A-T) is an autosomal recessive chromosome breakage disorder caused by mutations in the ATM gene. Typically, it presents in early childhood with progressive cerebellar dysfunction along with immunodeficiency and oculocutaneous telangiectasia. An increased risk of malignancy is also associated
    Phosphorylation of Hdmx mediates its Hdm2- and ATM-dependent degradation in response to DNA damage
    Pereg Y, et al.
    Proceedings of the National Academy of Sciences of the USA, 102(14), 5056-5061 (2005)
    Marta Viana-Pereira et al.
    PloS one, 6(5), e20588-e20588 (2011-06-04)
    High grade gliomas (HGG) are one of the leading causes of cancer-related deaths in children, and there is increasing evidence that pediatric HGG may harbor distinct molecular characteristics compared to adult tumors. We have sought to clarify the role of
    Armin M Gamper et al.
    Nucleic acids research, 41(22), 10334-10344 (2013-09-17)
    The kinase ATR is activated by RPA-coated single-stranded DNA generated at aberrant replicative structures and resected double strand breaks. While many hundred candidate ATR substrates have been identified, the essential role of ATR in the replicative stress response has impeded

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