{"product_id":"cst-48160t","title":"CST,  48160T, DNA Polymerase theta (POLQ) (153-5-1) Mouse Monoclonal Antibody","description":"Monoclonal Antibody for studying POLQ. Validated for Western Blotting,Immunoprecipitation. Available in 2 sizes. Highly specific and rigorously validated in-house, DNA Polymerase theta (POLQ) (153-5-1) Mouse Monoclonal Antibody (CST #48160) is ready to ship.\n\n\u003cb\u003eProduct Usage Information\u003c\/b\u003e\nWestern Blotting: 1:1000\nImmunoprecipitation: 1:100\n\u003cb\u003eStorage\u003c\/b\u003e\nSupplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg\/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at -20°C. Do not aliquot the antibody.\n\u003cb\u003eProtocol\u003c\/b\u003e\nAvailable protocols: Western Blotting, Immunoprecipitation\n\u003cb\u003eSpecificity \/ Sensitivity\u003c\/b\u003e\nDNA Polymerase theta (POLQ) (153-5-1) Mouse Monoclonal Antibody recognizes endogenous levels of total POLQ protein. By western blot, this antibody detects a band of unknown origin at approximately 260 kDa.\nSpecies Reactivity: Mouse\n\u003cb\u003eSource \/ Purification\u003c\/b\u003e\nMonoclonal antibody is produced by immunizing animals with recombinant protein specific to the carboxy terminus of human POLQ protein.\n\u003cb\u003eBackground\u003c\/b\u003e\nMammalian cells undergo DNA damage in response to various intrinsic and extrinsic forces, and signaling pathways are in place to sense and repair damaged DNA to avoid genome instability and mutation. Repair of toxic DNA double-strand breaks (DSBs) can occur through several pathways, and pathway choice may depend on the cell cycle phase and the nature of the DSB (1). The two main pathways for DSB repair areÂ classical non-homologous end joiningÂ (C-NHEJ) andÂ homologous recombinationÂ (HR).Â In addition, three error-prone pathways, single-strand annealing (SSA), microhomology-mediated end-joining (MMEJ), and polymerase theta-mediated end-joining (TMEJ) have been described (2). Exploiting DNA repair deficiencies in human cancer by targeting intact DNA repair pathways is a promising approach to cancer therapy. This approach has been successful with the use of poly (ADP-ribose) polymerase (PARP) inhibitors in HR-deficient cancer (3). DNA polymerase Î¸, encoded by theÂ Â gene, is a 290 kDa protein with an N-terminal helicase-like domain and a C-terminal DNA polymerase domain (4). ZEB1, an epithelial-mesenchymal transition (EMT) transcription factor, has been shown to regulate TMEJ by suppressing POLQ expression (5). DNA polymerase Î¸ is essential in TMEJ and is, therefore, an important target for drug development in HR-deficient cancers (6,7). Several inhibitors of DNA polymerase Î¸ are under investigation in pre-clinical and clinical trials (8,9).\n\u003cb\u003eAlternate Names\u003c\/b\u003e\nDKFZp781A0112; DNA polymerase eta; DNA polymerase theta; DPOLQ; epididymis secretory sperm binding protein; POLH; POLQ; polymerase (DNA directed), theta; polymerase (DNA) theta; PRO0327\n\n\u003cb\u003eSpecification\u003c\/b\u003e\n\nREACTIVITY: M\nSENSITIVITY: Endogenous\nMW (kDa): 280\nSource\/Isotype: Mouse IgG1 kappa","brand":"CST","offers":[{"title":"Default Title","offer_id":46800099999913,"sku":"48160T","price":0.99,"currency_code":"USD","in_stock":true}],"url":"https:\/\/iright.com\/products\/cst-48160t","provider":"Iright","version":"1.0","type":"link"}