ATM antibody (phosphorylated)

Catalog No. ABIN2666313

This Mouse Monoclonal antibody specifically detects ATM in BCA. It exhibits reactivity toward Human and Mouse.

Quick Overview for ATM antibody (phosphorylated) (ABIN2666313)

Target: ATM (Ataxia Telangiectasia Mutated (ATM))

Reactivity: Human, Mouse

Host: Mouse

Clonality: Monoclonal

Conjugate: This ATM antibody is un-conjugated

Application: Biochemical Assay (BCA)

Clone: 10H11-E12

Product Details anti-ATM Antibody

Binding Specificity: phosphorylated

Purification: The antibody was purified by affinity chromatography.

Isotype: IgG1 kappa

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

Buffer: phosphate-buffered solution, pH 7.2, containing 0.09 % sodium azide.

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Storage: 4 °C

Storage Comment: Upon receipt, store undiluted between 2°C and 8°C.

Target Details for ATM

Target: ATM (Ataxia Telangiectasia Mutated (ATM))

Alternative Name: ATM

Background: Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair. ATM is held inactive in unirradiated cells as a dimer or higher-order multimer. Cellular irradiation induces rapid intermolecular autophosphorylation of serine 1981 that causes dimer dissociation and initiates cellular ATM kinase activity. ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis, and DNA repair, including tumor suppressor proteins p53 and BRCA1, checkpoint kinase CHK2, checkpoint proteins RAD17 and RAD9, and DNA repair protein NBS1. 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.

Pathways: p53 Signaling, Apoptosis, DNA Damage Repair, Inositol Metabolic Process, Positive Regulation of Response to DNA Damage Stimulus