抗ATM抗体 | Anti-ATM Antibody

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	Western Blot: ATM Antibody [NB100-104] - Detection of ATM in HeLa nuclear extract using NB100-104. (30 sec. exposure)
	Immunocytochemistry/Immunofluorescence: ATM Antibody [NB100-104] - HeLa cells were fixed for 10 minutes using 10% formalin and then permeabilized for 5 minutes using 1X TBS + 0.05% Triton-X100. Then cells were incubated with anti-ATM (NB100-104) at a 1:100 dilution overnight at 4C and detected with an anti-rabbit Dylight 488 (Green) at a 1:500 dilution. Alpha tubulin was used as a co-stain at a 1:1000 dilution and detected with an anti-mouse Dylight 550 (Red) at a 1:500 dilution. Nuclei were counterstained with DAPI (Blue). Cells were imaged using a 40X objective.
	Immunohistochemistry-Paraffin: ATM Antibody [NB100-104] - Staining of human tonsil, germinal center and mantle zone.
	Flow Cytometry: ATM Antibody [NB100-104] - An intracellular stain was performed on HepG2 cells with ATM antibody NB100-104PE (blue) and a matched isotype control (orange). Cells were fixed with 4% PFA and then permeablized with 0.1% saponin.Cells were incubated in an antibody dilution of 5 ug/mL for 30 minutes at room temperature. Both antibodies were conjugated to Phycoerythrin.
	Western Blot: ATM Antibody [NB100-104] - Detection of ATM in Raji whole cell lysate.
	Flow Cytometry: ATM Antibody [NB100-104] - Analysis of PE conjugate of NB100-104. An intracellular stain was performed on HeLa cells with ATM antibody NB100-104PE (blue) and a matched isotype control NBP2-24893PE (orange). Cells were fixed with 4% PFA and then permeablized with 0.1% saponin. Cells

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Background

ATM (ataxia telangiectasia mutated kinase), the master regulator of DNA double-strand breaks (DSBs) repair pathway, is a serine/threonine protein kinase that act as DNA damage sensor by activating checkpoint signaling upon DSBs, apoptosis and genotoxic stresses. ATM activation involves its recruitment to DSBs through interaction with the MRE11-RAD50-NBS1 or MRN complex, followed by KAT5/TIP60 mediated acetylation. ATM recognizes the substrate consensus sequence [ST]-Q and phosphorylates 'Ser-139' of histone variant H2AX/H2AFX at DSBs, thereby regulating DNA damage response mechanism. ATM also implicates in vesicle and/or protein transport, T-cell development, gonads/neurological function, pre-B cell allelic exclusion, signal transduction, cell cycle control and act as a tumor suppressor. ATM exist as dimers or tetramers in inactive state and on DNA damage, autophosphorylation dissociates ATM into monomers rendering them catalytically active and binds/activates ABL1, SAPK, DYRK2, CHEK2, p53/TP53, FANCD2, NFKBIA, BRCA1, CTIP, nibrin (NBN), TERF1, RAD9 and DCLRE1C. ATM is an integral part of BASC complex (BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBN protein complex) and interacts with DCLRE1C, KAT8, KAT5, NABP2, ATMIN, CEP164, AP2B1, AP3B2, TELO2, TTI1, DDX1 etc. NUAK1/ARK5 mediated ATM phosphorylation and ATM autophosphorylation at Ser-367, Ser-1893, Ser-1981 correlates with DNA damage-regulated activation of the kinase. Defects in ATM are the cause of ataxia telangiectasia (AT), T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL), B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL), B-cell chronic lymphocytic leukemia (BCLL).

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