Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb

Phospho-ATM (Ser1981) (10H11.E

12) Mouse mAb
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  • 询价
  • Cell Signaling Technology已认证
  • USA
  • 2025年10月11日
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    • 详细信息
    • 技术资料
    • 抗体英文名

      Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb

    • 抗原

      synthetic phosphopeptide corresponding to residues around Ser1981 of human ATM

    • 应用范围

      W

    • 适应物种

      H

    • 库存

      大量

    • 供应商

      CST

    • 级别

      详见MSDS文件

    • 保质期

      详见说明书

    • 是否单克隆

      1

    • 保存条件

      -20°c

    • 规格

      100 ul (10 western blots)/300 ul (30 western blots)/carrier free & custom formulation / quantity

    规格:产品价格:¥请询价
    规格:100 ul (10 western blots)产品价格:¥请询价
    规格:300 ul (30 western blots)产品价格:¥请询价
    规格:carrier free & custom formulation / quantity产品价格:¥请询价

    pathway more info application references datasheet PDF MSDS PDF protocols

    Applications Key:  W=Western Blotting
    Reactivity Key:  H=Human
    Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

    Applications Reactivity Sensitivity MW (kDa) Isotype
    W H Endogenous 350 Mouse IgG1
    Protocols
    Specificity / Sensitivity

    Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb detects endogenous levels of ATM only when phosphorylated at Ser1981.

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues around Ser1981 of human ATM.

    Western Blotting

    Western Blotting

    Western blot analysis of extracts from M059J cells, untreated, treated with doxorubicin, or treated with bleomycin, using Phospho-ATM (Ser1981) (10H11.E12) Mouse mAb.

    Background

    Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair (1). Activation of ATM by autophosphorylation on Ser1981 occurs in response to exposed DNA double stranded breaks. ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis, and DNA repair. Known substrates include p53, Chk2, Chk1, CtIP, 4E-BP1, BRCA1, RPA3, H2A.X, SMC1, FANCD2, Rad17, Artemis, Nbs1, and the I-2 regulatory subunit of PP1 (1,2). Mutations in the corresponding ATM gene result in ataxia telangiectasia (AT), an autosomal recessive disease characterized by uncoordinated muscle movement and neurodegeneration. Cells from AT patients display defective DNA damage-induced checkpoint activation, sensitivity to radiation, and a higher frequency of chromosome breakage (3,4).

    1. Lee, J.H. and Paull, T.T. (2007) Oncogene 26, 7741-8.
    2. Tang, X. et al. (2008) Mol Cell Biol 28, 2559-66.
    3. Shiloh, Y. (1997) Annu Rev Genet 31, 635-62.
    4. Petrini, J.H. (2000) Curr Opin Cell Biol 12, 293-6.
    Application References

    Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know !

    Companion Products

    This product is sold under license, U.S. Patent Publication numbers 2003/0077661 and 2003/0157572, from St. Jude Childrens Research Hospital.


    For Research Use Only. Not For Use In Diagnostic Procedures.

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