ATM Antikörper (phosphorylated)

Produktnummer ABIN2666313

Dieser Maus Monoklonal Antikörper detektiert spezifisch ATM in BCA. Es zeigt Reaktivität gegenüber Proben von Human und Maus.

Kurzübersicht für ATM Antikörper (phosphorylated) (ABIN2666313)

Target: ATM (Ataxia Telangiectasia Mutated (ATM))

Reaktivität: Human, Maus

Wirt: Maus

Klonalität: Monoklonal

Konjugat: Dieser ATM Antikörper ist unkonjugiert

Applikation: Biochemical Assay (BCA)

Klon: 10H11-E12

Produktdetails anti-ATM Antikörper

Bindungsspezifität: phosphorylated

Aufreinigung: The antibody was purified by affinity chromatography.

Isotyp: IgG1 kappa

Anwendungsinformationen

Applikationshinweise: Optimal working dilution should be determined by the investigator.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

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

Konservierungsmittel: Sodium azide

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

Lagerung: 4 °C

Informationen zur Lagerung: Upon receipt, store undiluted between 2°C and 8°C.

Details zu ATM

Target: ATM (Ataxia Telangiectasia Mutated (ATM))

Andere Bezeichnung: ATM

Hintergrund: 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 Signalweg, Apoptose, DNA Reparatur, Inositol Metabolic Process, Positive Regulation of Response to DNA Damage Stimulus