ATM antibody (N-Term)

Catalog No. ABIN6242170

Product Details anti-ATM Antibody

Target: ATM (Ataxia Telangiectasia Mutated (ATM))

Binding Specificity: AA 5-34, N-Term

Reactivity: Human

Host: Rabbit

Clonality: Polyclonal

Conjugate: This ATM antibody is un-conjugated

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.

Immunogen: 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

Application Details

Application Notes: WB: 1:500. IHC-P: 1:50~100

Restrictions: For Research Use only

Handling

Format: Liquid

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

Expiry Date: 6 months

Target Details for ATM

Target: ATM (Ataxia Telangiectasia Mutated (ATM))

Alternative Name: ATM (ATM Products)

Background: 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.

Molecular Weight: 350687

NCBI Accession: NP_000042

UniProt: Q13315

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