RIP1 Antibody

Prouduct: We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality RIP1 Antibody. Functiong: Serine-threonine kinase which transduces inflammatory and cell-death signals (programmed necrosis) following death receptors ligation, activation of pathogen recognition receptors (PRRs), and DNA damage. Upon activation of TNFR1 by the TNF-alpha family cytokines, TRADD and TRAF2 are recruited to the receptor. Phosphorylates DAB2IP at 'Ser-728' in a TNF-alpha-dependent manner, and thereby activates the MAP3K5-JNK apoptotic cascade. Ubiquitination by TRAF2 via 'Lys-63'-link chains acts as a critical enhancer of communication with downstream signal transducers in the mitogen-activated protein kinase pathway and the NF-kappa-B pathway, which in turn mediate downstream events including the activation of genes encoding inflammatory molecules. Polyubiquitinated protein binds to IKBKG/NEMO, the regulatory subunit of the IKK complex, a critical event for NF-kappa-B activation. Interaction with other cellular RHIM-containing adapters initiates gene activation and cell death. RIPK1 and RIPK3 association, in particular, forms a necrosis-inducing complex. Summary: RIP1 Antibody: RIP1 (Receptor Interacting Protein), also known as RIPK1, is a crucial 74 kD adaptor kinase in several of stress-induced signaling pathways and on the crossroad of a cell’s decision to live or die. RIP1 contains an N-terminal region with homology to protein kinases, an intermediate domain capable of association with MAPKKK and a C-terminal region containing a death domain motif present in the Fas and TNFR1 intracellular domains. Full length RIP1 is important for signallling to NF-kappa-B, MAPKs and necrosis, whereas caspase-8 generates a C-terminal RIP1 cleavage fragment, promoting TNF-induced apoptosis. It is required for TNFRSF1A-mediated and TLR3-induced NF-kappa-B activation. RIP1-deficient mice fail to thrive, displaying extensive apoptosis in both lymphoid and adipose tissues and dying at 1-3 days of age.