Product nameAnti-RIP antibody
See all RIP primary antibodies
DescriptionRabbit polyclonal to RIP
Specificityab106393 reacts with RIP. It does not crossreact with other TKL Ser/Thr protein kinase family members.
Tested applicationsSuitable for: ICC/IF, WB, IHC-Pmore details
Species reactivityReacts with: Mouse, Rat, Human
Synthetic peptide corresponding to Human RIP (N terminal).
Database link: Q13546
- WB: Rat kidney lysate IHC-P: Mouse kidney tissue ICC/IF: Mouse kidney cells.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle.
Storage bufferPreservative: 0.02% Sodium azide
Concentration information loading...
PurityImmunogen affinity purified
Our Abpromise guarantee covers the use of ab106393 in the following tested applications.
|ICC/IF||Use a concentration of 20 µg/ml.|
|WB||Use a concentration of 1 - 2 µg/ml. Predicted molecular weight: 76 kDa.|
|IHC-P||Use a concentration of 2.5 µg/ml.|
FunctionEssential adapter molecule for the activation of NF-kappa-B. Following different upstream signals (binding of inflammatory cytokines, stimulation of pathogen recognition receptors, or DNA damage), particular RIPK1-containing complexes are formed, initiating a limited number of cellular responses. Upon TNFA stimulation RIPK1 is recruited to a TRADD-TRAF complex initiated by TNFR1 trimerization. There, it is ubiquitinated via 'Lys-63'-link chains, inducing its association with the IKK complex, and its activation through NEMO binding of polyubiquitin chains.
Sequence similaritiesBelongs to the protein kinase superfamily. TKL Ser/Thr protein kinase family.
Contains 1 death domain.
Contains 1 protein kinase domain.
modificationsProteolytically cleaved by caspase-8 during TNF-induced apoptosis. Cleavage abolishes NF-kappa-B activation and enhances pro-apototic signaling through the TRADD-FADD interaction.
Autophosphorylated on serine and threonine residues.
Ubiquitinated by 'Lys-11'-, 'Lys-48'-, 'Lys-63'- and linear-linked type ubiquitin. Polyubiquitination with 'Lys-63'-linked chains by TRAF2 induces association with the IKK complex. Deubiquitination of 'Lys-63'-linked chains and polyubiquitination with 'Lys-48'-linked chains by TNFAIP3 leads to RIPK1 proteasomal degradation and consequently to the termination of the TNF- or Linear polyubiquitinated; the head-to-tail polyubiquitination is mediated by the LUBAC complex. LPS-mediated activation of NF-kappa-B. Also ubiquitinated with 'Lys-11'-linked chains.
- Information by UniProt
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ab106393 has been referenced in 5 publications.
- Jia J et al. Recombinant PEP-1-SOD1 improves functional recovery after neural stem cell transplantation in rats with traumatic brain injury. Exp Ther Med 15:2929-2935 (2018). PubMed: 29599832
- Wójcik M et al. Expression of receptor interacting protein 1 and receptor interacting protein 3 oval cells in a rat model of hepatocarcinogenesis. Exp Ther Med 15:4448-4456 (2018). PubMed: 29731829
- Tan H et al. MicroRNA-24-3p Attenuates Myocardial Ischemia/Reperfusion Injury by Suppressing RIPK1 Expression in Mice. Cell Physiol Biochem 51:46-62 (2018). PubMed: 30439713
- Jackson R et al. Paracrine Engineering of Human Cardiac Stem Cells With Insulin-Like Growth Factor 1 Enhances Myocardial Repair. J Am Heart Assoc 4:e002104 (2015). WB . PubMed: 26363004
- Kim JE et al. LIM kinase-2 induces programmed necrotic neuronal death via dysfunction of DRP1-mediated mitochondrial fission. Cell Death Differ : (2014). PubMed: 24561342