ATM anticorps (AA 1974-1988)

N° du produit ABIN6655681

Détail du produit anti-ATM anticorps

Antigène: ATM (Ataxia Telangiectasia Mutated (ATM))

Épitope: AA 1974-1988

Reactivité: Humain

Hôte: Souris

Clonalité: Monoclonal

Conjugué: Cet anticorp ATM est non-conjugé

Application: Western Blotting (WB), Immunohistochemistry (IHC), ELISA, Flow Cytometry (FACS)

Réactivité croisée: Humain, Souris

Purification: This Protein A Purified Mab antibody is directed against human ATM and is useful in determining its presence by immunohistochemistry. This monoclonal anti-ATM antibody recognizes the phosphorylated form of the protein in native and over-expressed proteins found in various tissues and extracts.  Reactivity is observed against human and mouse ATM.  Cross reactivity with ATM from other mammalian sources has not been tested.

Immunogène:

Immunogen: This antibody was produced from a synthetic peptide S-L-A-F-E-E-G-Sp-Q-S-T-T-I-S-S corresponding to aa 1974-1988 of human ATM.

Immunogen Type: Peptide

Clone: 7C10D8

Isotype: IgG2a

Information d'application

Indications d'application:

Immunohistochemistry Dilution: 1:100 - 1:500

Application Note: This Anti-ATM Protein Kinase pS1981 (MOUSE) Monoclonal Antibody clone has been optimized for IHC, but may also be used for western blotting, flow cytometry, immunoprecipitation, or immunofluorescence microscopy. Indirect immunoperoxidase staining on formaldehyde-fixed, de-paraffinized tissue sections and/or formalin-fixed cultured cells are recommended when using this antibody as described in Bartkova et al 2005.  Product p/n 200-301-400 produced from clone 10H11.E12 has been optimized for WB, IP and IF.

ELISA Dilution: 1:10,000 - 1:50,000

Flow Cytometry Dilution: User Optimized

Western Blot Dilution: 1:500- 1:2,000

Restrictions: For Research Use only

Stockage

Format: Liquid

Buffer:

Buffer: 0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2

0.01 % (w/v) Sodium Azide

Stabilizer: None

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: RT,4 °C,-20 °C

Stockage commentaire: Store vial at -20° C prior to opening. Aliquot contents and freeze at -20° C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4° C as an undiluted liquid. Dilute only prior to immediate use.

Références pour anticorps anti-ATM (ABIN6655681)

Rosina, Langone, Giuliani, Cerquone Perpetuini, Reggio, Calderone, Fuoco, Castagnoli, Gargioli, Cesareni: "Osteogenic differentiation of skeletal muscle progenitor cells is activated by the DNA damage response." dans: Scientific reports, Vol. 9, Issue 1, pp. 5447, (2019) (PubMed).

Emery, Gopalan, Wood, Chow, Battelli, George, Blaszyk, Florman, Yun: "Expression and function of ABCG2 and XIAP in glioblastomas." dans: Journal of neuro-oncology, Vol. 133, Issue 1, pp. 47-57, (2018) (PubMed).

Sinha, Qin, Li: "A p53/ARF-dependent anticancer barrier activates senescence and blocks tumorigenesis without impacting apoptosis." dans: Molecular cancer research : MCR, Vol. 13, Issue 2, pp. 231-8, (2016) (PubMed).

Liu, Xu, OPrey, Lao, Joshi, Long, OPrey, Croft, Beaumatin, Baudot, Mrschtik, Rosenfeldt, Zhang, Gillespie, Ryan: "Loss of autophagy causes a synthetic lethal deficiency in DNA repair." dans: Proceedings of the National Academy of Sciences of the United States of America, Vol. 112, Issue 3, pp. 773-8, (2015) (PubMed).

Phesse, Myant, Cole, Ridgway, Pearson, Muncan, van den Brink, Vousden, Sears, Vassilev, Clarke, Sansom: "Endogenous c-Myc is essential for p53-induced apoptosis in response to DNA damage in vivo." dans: Cell death and differentiation, Vol. 21, Issue 6, pp. 956-66, (2014) (PubMed).

Broering, Alavattam, Sadreyev, Ichijima, Kato, Hasegawa, Camerini-Otero, Lee, Andreassen, Namekawa: "BRCA1 establishes DNA damage signaling and pericentric heterochromatin of the X chromosome in male meiosis." dans: The Journal of cell biology, Vol. 205, Issue 5, pp. 663-75, (2014) (PubMed).

Shamma, Suzuki, Hayashi, Kobayashi, Sasaki, Nishiuchi, Doki, Okamoto, Kohno, Muranaka, Kitajima, Yamamoto, Takahashi: "ATM mediates pRB function to control DNMT1 protein stability and DNA methylation." dans: Molecular and cellular biology, Vol. 33, Issue 16, pp. 3113-24, (2013) (PubMed).

Parikh, Shuck, Nguyen, Herron, Donehower: "Mouse tissues that undergo neoplastic progression after K-Ras activation are distinguished by nuclear translocation of phospho-Erk1/2 and robust tumor suppressor responses." dans: Molecular cancer research : MCR, Vol. 10, Issue 6, pp. 845-55, (2012) (PubMed).

Schwab, Smith, Dressler: "Arrested spermatogenesis and evidence for DNA damage in PTIP mutant testes." dans: Developmental biology, Vol. 373, Issue 1, pp. 64-71, (2012) (PubMed).

Lantuejoul, Raynaud, Salameire, Gazzeri, Moro-Sibilot, Soria, Brambilla, Brambilla: "Telomere maintenance and DNA damage responses during lung carcinogenesis." dans: Clinical cancer research : an official journal of the American Association for Cancer Research, Vol. 16, Issue 11, pp. 2979-88, (2010) (PubMed).

Navaraj, Finnberg, Dicker, Yang, Matthew, El-Deiry: "Reduced cell death, invasive and angiogenic features conferred by BRCA1-deficiency in mammary epithelial cells transformed with H-Ras." dans: Cancer biology & therapy, Vol. 8, Issue 24, pp. 2417-44, (2010) (PubMed).

Leemput, Masson, Bigot, Errachid, Dansault, Provost, Gadin, Aoufouchi, Menasche, Abitbol: "ATM localization and gene expression in the adult mouse eye." dans: Molecular vision, Vol. 15, pp. 393-416, (2009) (PubMed).

Raynaud, Jang, Nuciforo, Lantuejoul, Brambilla, Mounier, Olaussen, André, Morat, Sabatier, Soria: "Telomere shortening is correlated with the DNA damage response and telomeric protein down-regulation in colorectal preneoplastic lesions." dans: Annals of oncology : official journal of the European Society for Medical Oncology, Vol. 19, Issue 11, pp. 1875-81, (2008) (PubMed).

Bartkova, Bakkenist, Rajpert-De Meyts, Skakkebaek, Sehested, Lukas, Kastan, Bartek: "ATM activation in normal human tissues and testicular cancer." dans: Cell cycle (Georgetown, Tex.), Vol. 4, Issue 6, pp. 838-45, (2006) (PubMed).

Kitagawa, Bakkenist, McKinnon, Kastan: "Phosphorylation of SMC1 is a critical downstream event in the ATM-NBS1-BRCA1 pathway." dans: Genes & development, Vol. 18, Issue 12, pp. 1423-38, (2004) (PubMed).

Bakkenist, Kastan: "DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation." dans: Nature, Vol. 421, Issue 6922, pp. 499-506, (2003) (PubMed).

Détails sur ATM

Antigène: ATM (Ataxia Telangiectasia Mutated (ATM))

Autre désignation: ATM (ATM Produits)

Synonymes: anticorps ATM, anticorps Atm, anticorps CG6535, anticorps Dmel\\CG6535, anticorps Tefu, anticorps atm, anticorps atm/tefu, anticorps dATM, anticorps tef, anticorps Xatm, anticorps at1, anticorps atdc, anticorps tel1, anticorps telo1, anticorps AT1, anticorps ATA, anticorps ATC, anticorps ATD, anticorps ATDC, anticorps ATE, anticorps TEL1, anticorps TELO1, anticorps AI256621, anticorps C030026E19Rik, anticorps telomere fusion, anticorps ATM serine/threonine kinase L homeolog, anticorps ATM serine/threonine kinase, anticorps ataxia telangiectasia mutated, anticorps ataxia telangiectasia mutated (atm), anticorps serine/threonine-protein kinase ATM, anticorps tefu, anticorps atm.L, anticorps atm, anticorps ATM, anticorps EDI_100660, anticorps CpipJ_CPIJ001772, anticorps BDBG_08252, anticorps PAAG_02532, anticorps MCYG_05088, anticorps VDBG_06833, anticorps ACLA_015700, anticorps LOC5565620, anticorps MGYG_07634, anticorps PGTG_14279, anticorps Atm

Sujet:

Synonyms: mouse anti-ATM antibody, mouse anti-ATMpS1981 antibody, mouse anti- ATM pS1981 antibody, DKFZp781A0353 antibody, Human phosphatidylinositol 3 kinase homolog antibody, MGC74674 antibody, Serine protein kinase ATM antibody, T cell prolymphocytic leukemia antibody

Background: Anti ATM pS1981 Antibody recognizes the product of the ATM gene that is mutated in the hereditary disease ataxia-telangiectasia. ATM codes for a protein kinase that acts as a master regulator of cellular responses to DNA double-strand breaks. ATM is normally inactive and the question of how it is activated in the event of DNA damage (due to ionizing radiation for instance) is central to understanding its function. ATM protein is now shown to be present in undamaged cells as an inactive dimer. Low doses of ionizing radiation, which induce only a few DNA breaks, activate at least half of the total ATM protein present, possibly in response to changes in chromatin structure.  The ATM gene encodes a 370- kDa protein that belongs to the phosphoinositide 3-kinase (PI(3)K) superfamily, but which phosphorylates proteins rather than lipids. The 350-amino-acid kinase domain at the carboxy terminus of this large protein is the only segment of ATM with an assigned function. Exposure of cells to IR triggers ATM kinase activity, and this function is required for arrests in G1, S and G2 phases of the cell cycle. Several substrates of the ATM kinase participate in these IR-induced cell-cycle arrests. These include p53, Mdm2 and Chk2 in the G1 checkpoint, Nbs1, Brca1, FancD2 and SMC1 in the transient IR-induced S-phase arrest, and Brca1 and hRad17 in the G2/M checkpoint. See Bakkenist, C. J. & Kastan, M. B. Nature 421, 499-506 (2003) for a complete presentation of this antibody's specificity and utility.

Gene Name: ATM

ID gène: 472

UniProt: Q13315

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