#151333

Anti-ATM [ATM 11G12]

Cat. #151333

Anti-ATM [ATM 11G12]

Cat. #: 151333

Sub-type: Primary antibody

Unit size: 100 ug

Availability: 1-2 weeks

Target: Ataxia Telangiesctasia Mutated (ATM)

Class: Monoclonal

Application: IF ; IP ; WB

Reactivity: Human

Host: Mouse

£300.00

This fee is applicable only for non-profit organisations. If you are a for-profit organisation or a researcher working on commercially-sponsored academic research, you will need to contact our licensing team for a commercial use license.

Contributor

Institute: University of Birmingham

Tool Details
Target Details
Applications
Handling
References

Tool Details

*FOR RESEARCH USE ONLY

  • Name: Anti-ATM [ATM 11G12]
  • Clone: ATM 11G12
  • Tool sub type: Primary antibody
  • Class: Monoclonal
  • Conjugation: Unconjugated
  • Molecular weight: 370 kDa
  • Reactivity: Human
  • Host: Mouse
  • Application: IF ; IP ; WB
  • Description: The ATM protein is a member of the phosphatidylinositol-3 kinase family of proteins that respond to DNA damage by phosphorylating key substrates involved in DNA repair and/or cell cycle control. It is thought that the activation of ATM by autophosphorylation might be the initiating event of cellular responses to irradiation. The classic form of ataxia telangiectasia, an autosomal recessive cerebellar ataxia, results from the presence of two truncating ATM mutations, leading to a total loss of the ATM protein.
  • Immunogen: Residues 992-1144 of ATM fusion protein
  • Isotype: IgG1
  • Myeloma used: Sp2/0-Ag14

Target Details

  • Target: Ataxia Telangiesctasia Mutated (ATM)
  • Molecular weight: 370 kDa
  • Target background: The ATM protein is a member of the phosphatidylinositol-3 kinase family of proteins that respond to DNA damage by phosphorylating key substrates involved in DNA repair and/or cell cycle control. It is thought that the activation of ATM by autophosphorylation might be the initiating event of cellular responses to irradiation. The classic form of ataxia telangiectasia, an autosomal recessive cerebellar ataxia, results from the presence of two truncating ATM mutations, leading to a total loss of the ATM protein.

Applications

  • Application: IF ; IP ; WB

Handling

  • Format: Liquid
  • Concentration: 1 mg/ml
  • Unit size: 100 ug
  • Storage buffer: PBS with 0.02% azide
  • Storage conditions: -80° C
  • Shipping conditions: Shipping at 4° C

References

  • Dynamics of DNA damage induced pathways to cancer.
  • Tian et al. 2013. PLoS One. 8(9):e72303. PMID: 24023735.
  • Reiman et al. 2011. Br J Cancer. 105(4):586-91. PMID: 21792198.
  • Lymphoid tumours and breast cancer in ataxia telangiectasia
  • substantial protective effect of residual ATM kinase activity against childhood tumours.
  • Dutton et al. 2007. Blood. 109(6):2597-603. PMID: 17148591.
  • Bmi-1 is induced by the Epstein-Barr virus oncogene LMP1 and regulates the expression of viral target genes in Hodgkin lymphoma cells.
  • Clements et al. 2004. DNA Repair (Amst). 3(11):1493-502. PMID: 15380105.
  • The ataxia-oculomotor apraxia 1 gene product has a role distinct from ATM and interacts with the DNA strand break repair proteins XRCC1 and XRCC4.
  • Starczynski et al. 2003. Am J Pathol. 163(2):423-32. PMID: 12875964.
  • Variations in ATM protein expression during normal lymphoid differentiation and among B-cell-derived neoplasias.