ATM anticorps (N-Term)

N° du produit ABIN6242170

Détail du produit anti-ATM anticorps

Antigène: ATM (Ataxia Telangiectasia Mutated (ATM))

Épitope: AA 5-34, N-Term

Reactivité: Humain

Hôte: Lapin

Clonalité: Polyclonal

Conjugué: Cet anticorp ATM est non-conjugé

Application: Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))

Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.

Immunogène: This ATM antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 5~34 amino acids from the N-terminal region of human ATM.

Clone: RB3111-3112

Isotype: Ig Fraction

Information d'application

Indications d'application: WB: 1:500. IHC-P: 1:50~100

Restrictions: For Research Use only

Stockage

Format: Liquid

Buffer: Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) 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,-20 °C

Date de péremption: 6 months

Détails sur ATM

Antigène: ATM (Ataxia Telangiectasia Mutated (ATM))

Autre désignation: ATM (ATM Produits)

Sujet: ATM is involved in signal transduction, cell cycle control and DNA repair, and may function as a tumor suppressor. It is necessary for activation of ABL1 and SAPK, and phosphorylates p53, NFKBIA, BRCA1, CTIP, NIBRIN (NBS1), TERF1, and RAD9. This protein has potential roles in vesicle and/or protein transport, T-cell development, gonad and neurological function. ATM is also part of the BRCA1-associated genome surveillance complex. ATM is induced by ionizing radiation. Defects in ATM are the cause of ataxia talangiectasia (AT), also known as Louis-Bar syndrome, a rare recessive disorder characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. About 30 % of AT patients develop lymphomas and leukemias. Defects in ATM also contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. Defects in ATM also contribute to B-cell non-Hodgkin's lymphomas, and to B-cell chronic lymphocytic leukemia, a disease characterized by accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.

Poids moléculaire: 350687

NCBI Accession: NP_000042

UniProt: Q13315

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