{"product_id":"cst-15828s","title":"CST,  15828S, RIP3 (D8J3L) Rabbit Monoclonal Antibody","description":"Monoclonal Antibody for studying RIPK3 mouse. Validated for Western Blotting,Immunoprecipitation. Available in 2 sizes. Highly specific and rigorously validated in-house, RIP3 (D8J3L) Rabbit Monoclonal Antibody (CST #15828) 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. For a carrier free (BSA and azide free) version of this product see product # 92131 .\n\u003cb\u003eProtocol\u003c\/b\u003e\nAvailable protocols: Western Blotting, Immunoprecipitation\n\u003cb\u003eSpecificity \/ Sensitivity\u003c\/b\u003e\nRIP3 (D8J3L) Rabbit Monoclonal Antibody recognizes endogenous levels of total RIP3 protein from mouse and rat.\nSpecies Reactivity: Mouse, Rat\n\u003cb\u003eSource \/ Purification\u003c\/b\u003e\nMonoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding His411 of mouse RIP3 protein.\n\u003cb\u003eBackground\u003c\/b\u003e\nThe receptor-interacting protein (RIP) family of serine-threonine kinases (RIP, RIP2, RIP3, and RIP4) are important regulators of cellular stress that trigger pro-survival and inflammatory responses through the activation of NF-κB, as well as pro-apoptotic pathways (1). In addition to the kinase domain, RIP contains a death domain responsible for interaction with the death domain receptor Fas and recruitment to TNF-R1 through interaction with TRADD (2,3). RIP-deficient cells show a failure in TNF-mediated NF-κB activation, making the cells more sensitive to apoptosis (4,5). RIP also interacts with TNF-receptor-associated factors (TRAFs) and can recruit IKKs to the TNF-R1 signaling complex via interaction with NEMO, leading to IκB phosphorylation and degradation (6,7). Overexpression of RIP induces both NF-κB activation and apoptosis (2,3). Caspase-8-dependent cleavage of the RIP death domain can trigger the apoptotic activity of RIP (8). Receptor-interacting protein 3 (RIP3) was originally found to interact with RIP and the TNF receptor complex to induce apoptosis and activation of NF-κB (9,10). It has subsequently been shown that the association between RIP and RIP3 is a key component of a signaling pathway that results in programmed necrosis (necroptosis), a necrotic-like cell death induced by TNF in the presence of caspase inhibitors (11-13). RIP3 is phosphorylated at Ser227 and targets the phosphorylation of mixed lineage kinase domain-like protein (MLKL), which is critical for necroptosis (14).\n\u003cb\u003eAlternate Names\u003c\/b\u003e\n2610528K09Rik; AW107945; mRIP3; receptor interacting protein 3; Receptor-interacting protein 3; receptor-interacting serine-threonine kinase 3; Receptor-interacting serine\/threonine-protein kinase 3; RIP-3; RIP-like protein kinase 3; Rip3; Ripk3\n\n\u003cb\u003eSpecification\u003c\/b\u003e\n\nREACTIVITY: M R\nSENSITIVITY: Endogenous\nMW (kDa): 46-62\nSource\/Isotype: Rabbit IgG","brand":"CST","offers":[{"title":"Default Title","offer_id":46801049190569,"sku":"15828S","price":0.99,"currency_code":"USD","in_stock":true}],"url":"https:\/\/iright.com\/products\/cst-15828s","provider":"Iright","version":"1.0","type":"link"}