Anti-ATM Antibody

Control
HeLa nuclear extract

Evaluated by Western Blotting in HeLa nuclear extract.

Western Blotting Analysis: A 1:500 dilution of this antibody detected ATM in 10 µg of HeLa nuclear extract.

Anti-ATM Antibody detects level of ATM & has been published & validated for use in WB & IF.

Research Category
Epigenetics & Nuclear Function

Research Sub Category
Nuclear Receptors

Western Blotting Analysis: A 1:5,000 dilution from a representative lot detected ATM in 10 µg of HeLa nuclear extract.
Immunocytochemistry Analysis: A representative lot detected ATM in HeLa and NIH/3T3 cells.
Immunocytochemistry Analysis: 2 µg/mL from a representative lot detected ATM in NIH/3T3 cells.

Detects ATM.

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>260 kDa observed. Uncharacterized band(s) may appear in some lysates.

ATM (Ataxia Telangiectasia Mutated kinase) and ATR (Ataxia Telangiectasia and Rad3-related kinase) are related kinases that regulate cell cycle checkpoints and DNA repair. ATM is activated in response to DNA damage and serves to arrest further cell division before the damage can be repaired. Mutation in the ATM gene results in the autosomal recessive disease ataxia telangiectasia (AT). The identified substrates for ATM include p53, p95/NBS1, MDM2, Chk2, BRCA1, CtIP, 4E-BP1 and Chk1. ATM activates p53, increasing p21/Cip1/Waf1 levels, thus blocking activation of Cdk2. That results in Rb hypophosphorylation and blockage of the G1/S transition. Separately, ATM also phosphorylates and activates Chk1, which phosphorylates Cdc25C. This inactivates Cdc25C and prevents it from dephosphorylating the inhibitory phosphotyrosine residue on cdc2/Cdk1, thus preventing the G2/M transition. The complex phenotype of cells derived from patients with AT suggests that ATM has additional cellular substrates. In unirradiated cells, ATM is present as an inactive homodimer or multimer. Double-stranded breaks in DNA caused by ionizing radiation cause rapid ATM kinase activation through dissociation of this complex and ATM autophosphorylation at Ser1981.

Epitope: Abl-interacting domain

KLH-conjugated synthetic peptide corresponding to sequence derived from the Abl-interacting domain of human ATM.

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Antigen Affinity Purified

Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Stable for 1 year at 2-8°C from date of receipt.
Handling Recommendations: Upon receipt, and prior to removing the cap, centrifuge the vial and gently mix the solution.

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