Anti-ATM [ATM 11G12]

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 […]

Contributors

Institute
University of Birmingham
Cat. #: 151333
Tool sub type: Primary antibody
Unit size: 100 ug
Research Fields: Cancer;Cell biology;Genetics
Application: IF ; IP ; WB
Target: Ataxia Telangiesctasia Mutated (ATM)
Reactivity: Human
Clone: ATM 11G12
Host: Mouse
Class: Monoclonal
Product 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.
Conjugation: Unconjugated
Isotype: IgG1
Molecular weight: 370 kDa
Immunogen: Residues 992-1144 of ATM fusion protein
Myeloma used: Sp2/0-Ag14
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.
Format: Liquid
Concentration: 1 mg/ml
Storage buffer: PBS with 0.02% azide
Storage conditions: -80° C
Shipping conditions: Dry ice
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.

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