ATM antibody (phosphorylated) (PE)

Catalog No. ABIN2662388

Product Details anti-ATM Antibody (PE)

Target: ATM (Ataxia Telangiectasia Mutated (ATM))

Binding Specificity: phosphorylated

Reactivity: Human, Mouse

Host: Mouse

Clonality: Monoclonal

Conjugate: This ATM antibody is conjugated to PE

Application: Flow Cytometry (FACS)

Purification: The antibody was purified by affinity chromatography and conjugated with PE under optimal conditions. The solution is free of unconjugated PE and unconjugated antibody.

Clone: 10H11-E12

Isotype: IgG1 kappa

Application Details

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

Restrictions: For Research Use only

Handling

Concentration: 0.2 mg/mL

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.

Handling Advice: Protect from prolonged exposure to light. Do not freeze.

Storage: 4 °C

Storage Comment: The antibody solution should be stored undiluted between 2°C and 8°C.

Target Details for ATM

Target: ATM (Ataxia Telangiectasia Mutated (ATM))

Alternative Name: ATM (ATM Products)

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