AVANTI POLAR LIPIDS , CYGNUS , LARODAN , ADIPOGEN , MYBIOSOURCE , SERVA NORDMARK, BIOWORLD, EDGEBIO , PANREAC APPLICHEM
Ajouter au panier
Le produit a été ajouté au panier
Le stock est insuffisant. unités ont été rajoutées au panier
En rupture de stock
Quantité minimum d'achat
La quantité minimum d'achat n'est pas atteinte
photos non contractuelles
Product description: Receptor interacting protein (RIP) kinases constitute a family of seven members, all of which contain a kinase domain (KD). They are crucial regulators of cell survival and death. RIP1, the first member of the family, is highly conserved in vertebrate evolution. RIP1 and RIP2 bear a C-terminal domain belonging to the death domain (DD) and a caspase recruitment domain (CARD), allowing recruitment to large protein complexes initiating different signaling pathways. Human RIP1 is 68% identical to mouse RIP1, and the greatest similarity is in the DD. RIP1-DD is important for binding to other death receptors, such as tumor necrosis factor (TNF)-R1, TRAIL-R1 and TRAIL-R2, and to DD-containing adaptor proteins such as TNF-receptor-associated death domain (TRADD) and FADD. RIP1 is constitutively expressed in many tissues. However, TNF treatment and T-cell activation can also induce RIP1 expression. Full-length RIP1 is important for signaling to NF-B, MAPKs and necrosis, whereas caspase-8 generated C-terminal RIP1 cleavage fragment promotes apoptosis as a positive feedback loop. RIP1 thus integrates several different upstream signals to initiate a limited number of cellular responses. RIP1 is a crucial adaptor kinase in several of the stress-induced signaling pathways. The imbalance between cell survival and death, a key feature of many neoplastic, degenerative, inflammatory, and autoiummune diseases, may be caused by aberrant reactive oxygen species (ROS) turnover, which can be regulated by death receptors (DRs) and their effector pathways. Involved in the transduction of TNF signaling. TNF stimulation induces binding of RIPK1-TRADD-TRAF2-TRAF5 complex to TNFR1. TRAF proteins then catalyze the 'Lys-63'-linked polyubiquitination of RIPK1, inducing RIPK1 association with the IKK complex, which is subsequently activated, leading ultimately to the activation of NF-kappa-B. The inflammatory response is kept transient by the action of the NF-kappa-B target gene product TNFAIP3. TNFAIP3 is recruited to RIPK1 within a complex comprising also RNF11, ITCH and TAX1BP1. TNFAIP3 deubiquitinates 'Lys-63'-polyubiquitin chains on RIPK1 and catalyzes the formation of 'Lys-48'-polyubiquitin chains. This leads to RIPK1 proteosomal degradation and consequently to the termination of the TNF- or LPS-mediated activation of NF-kappa-B.
Alternate Names/Synonyms: RIP; RIPK1; RIP-1; EC=22.214.171.124; Cell Death Protein RIP; Receptor-interacting Protein 1; Serine/Threonine-Protein Kinase RIP; Receptor-interacting Serine/Threonine-Protein Kinase 1
Product Type: Monoclonal Antibody
Isotype: Mouse IgG2b kappa
Immunogen: Recombinant human His/ABD-RIP1 protein purified from E. coli.
Applications: IP, WB
Species Crossreactivity: Human, Mouse, Rat
Formulation: Liquid. HEPES with 0.15M NaCl, 0.01% BSA, 0.03% sodium azide, and 50% glycerol.
Long Term Storage: -20°C
Shipping: BLUE ICE
Use & Stability: Stable for at least 1 year after receipt when stored at -20°C.
Veuillez saisir les champs obligatoires!