Anti-ATM antibody (ab47575)
- Product nameAnti-ATM antibodySee all ATM primary antibodies ...
- DescriptionRabbit polyclonal to ATM
- SpecificityThis antibody detects endogenous levels of total ATM protein.
- Tested applicationsIHC-P, ELISA, WB, ICC/IF more details
- Species reactivityReacts with: Mouse, Human
Synthetic non-phosphopeptide derived from human ATM around the phosphorylation site of serine 1981 (E-G-SP-Q-S).
- Positive controlIHC-P: Human breast carcinoma tissue.
- Storage instructionsStore at -20°C. Stable for 12 months at -20°C
- Storage bufferPreservative: 0.02% Sodium Azide
Constituents: 50% Glycerol, PBS, 150mM Sodium chloride, pH 7.4
- Concentration information loading...
- PurityImmunogen affinity purified
- Purification notesThe antibody was affinity purified from rabbit antiserum by affinity chromatography using epitope specific immunogen.
- Clonality Polyclonal
- Research Areas
Our Abpromise guarantee covers the use of ab47575 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|IHC-P||IHC-P: Use at an assay dependent dilution.|
|WB||WB: Use a concentration of 2 µg/ml. Use under non reducing condition. Detects a band of approximately 350 kDa (predicted molecular weight: 350 kDa).|
- FunctionSerine/threonine protein kinase which activates checkpoint signaling upon double strand breaks (DSBs), apoptosis and genotoxic stresses such as ionizing ultraviolet A light (UVA), thereby acting as a DNA damage sensor. Recognizes the substrate consensus sequence [ST]-Q. Phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at double strand breaks (DSBs), thereby regulating DNA damage response mechanism. Also plays a role in pre-B cell allelic exclusion, a process leading to expression of a single immunoglobulin heavy chain allele to enforce clonality and monospecific recognition by the B-cell antigen receptor (BCR) expressed on individual B lymphocytes. After the introduction of DNA breaks by the RAG complex on one immunoglobulin allele, acts by mediating a repositioning of the second allele to pericentromeric heterochromatin, preventing accessibility to the RAG complex and recombination of the second allele. Also involved in signal transduction and cell cycle control. May function as a tumor suppressor. Necessary for activation of ABL1 and SAPK. Phosphorylates p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. May play a role in vesicle and/or protein transport. Could play a role in T-cell development, gonad and neurological function. Plays a role in replication-dependent histone mRNA degradation. Binds DNA ends.
- Tissue specificityFound in pancreas, kidney, skeletal muscle, liver, lung, placenta, brain, heart, spleen, thymus, testis, ovary, small intestine, colon and leukocytes.
- Involvement in diseaseDefects in ATM are the cause of ataxia telangiectasia (AT) [MIM:208900]; also known as Louis-Bar syndrome, which includes four complementation groups: A, C, D and E. This rare recessive disorder is characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. AT patients have a strong predisposition to cancer; about 30% of patients develop tumors, particularly lymphomas and leukemias. Cells from affected individuals are highly sensitive to damage by ionizing radiation and resistant to inhibition of DNA synthesis following irradiation.
Note=Defects in ATM 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. The clinical course is highly aggressive, with poor response to chemotherapy and short survival time. TPLL occurs both in adults as a sporadic disease and in younger AT patients.
Note=Defects in ATM contribute to B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL).
Note=Defects in ATM contribute to B-cell chronic lymphocytic leukemia (BCLL). BCLL is the commonest form of leukemia in the elderly. It is characterized by the accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.
- Sequence similaritiesBelongs to the PI3/PI4-kinase family. ATM subfamily.
Contains 1 FAT domain.
Contains 1 FATC domain.
Contains 1 PI3K/PI4K domain.
- DomainThe FATC domain is required for interaction with KAT5.
modificationsPhosphorylated by NUAK1/ARK5. Autophosphorylation on Ser-367, Ser-1893, Ser-1981 correlates with DNA damage-mediated activation of the kinase.
Acetylation, on DNA damage, is required for activation of the kinase activity, dimer-monomer transition, and subsequent autophosphorylation on Ser-1981. Acetylated in vitro by KAT5/TIP60.
- Cellular localizationNucleus. Cytoplasmic vesicle. Primarily nuclear. Found also in endocytic vesicles in association with beta-adaptin.
- A-T mutated antibodyA-T mutated homolog antibodyAT mutated antibody
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Anti-ATM antibody images
ab47575 (1/50) staining ATM in paraffin embedded human breast carcinoma tissue. Right hand panel represents a negative control for which the primary antibody was pre-incubated with the immunizing (blocking) peptide.
ab47575 (1/200) detecting ATM in HeLa cells (green). Cells were fixed in paraformaldehyde and counterstained with DAPI (red) in order to highlight the nucleus. Please refer to abreview for further experimental details.
All lanes : Anti-ATM antibody (ab47575)
Lane 1 : Colon cancer lysate (human)
Lane 2 : U2OS lysate (human)
Lane 3 : Renal Cancer Cell Line (Human)
Lysates/proteins at 20 µg per lane.
Swine anti rabbit-HRP at 1/5000 dilution
developed using the ECL technique
Performed under reducing conditions.
Predicted band size : 350 kDa
Observed band size : 350 kDa
Exposure time : 6 minutes
This image is courtesy of an Abreview submitted by Antibody Solutions
References for Anti-ATM antibody (ab47575)
ab47575 has not yet been referenced specifically in any publications.