ATM anticorps (phosphorylated)

N° du produit ABIN2666313

Cet anticorps Souris Monoclonal détecte spécifiquement ATM dans BCA. Il présente une réactivité envers Humain et Souris.

Aperçu rapide pour ATM anticorps (phosphorylated) (ABIN2666313)

Antigène: ATM (Ataxia Telangiectasia Mutated (ATM))

Reactivité: Humain, Souris

Hôte: Souris

Clonalité: Monoclonal

Conjugué: Cet anticorp ATM est non-conjugé

Application: Biochemical Assay (BCA)

Clone: 10H11-E12

Détail du produit anti-ATM anticorps

Épitope: phosphorylated

Purification: The antibody was purified by affinity chromatography.

Isotype: IgG1 kappa

Information d'application

Indications d'application: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Stockage

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

Agent conservateur: Sodium azide

Précaution d'utilisation: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Stock: 4 °C

Stockage commentaire: Upon receipt, store undiluted between 2°C and 8°C.

Détails sur ATM

Antigène: ATM (Ataxia Telangiectasia Mutated (ATM))

Autre désignation: ATM

Sujet: 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: Signalisation p53, Apoptose, Réparation de l'ADN, Inositol Metabolic Process, Positive Regulation of Response to DNA Damage Stimulus