Product Pathways - NF-kB Signaling
RIP (D94C12) XP® Rabbit mAb #3493
|3493S||100 µl (10 western blots)||---||In Stock||---|
|3493P||40 µl (4 western blots)||---||In Stock||---|
|3493||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat, Hamster, Monkey||Endogenous||78||Rabbit|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-IC=Immunofluorescence (Immunocytochemistry), F=Flow Cytometry
Specificity / Sensitivity
RIP (D94C12) XP® Rabbit mAb detects endogenous levels of total RIP (RIP1) protein. It has not been shown to cross-react with other RIP family members.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu190 of human RIP.
Western blot analysis of extracts from various cell lines using RIP (D94C12) XP® Rabbit mAb.
Western blot analysis of extracts from HeLa cells, untransfected or transfected with human RIP construct, using RIP (D94C12) XP® Rabbit mAb.
Flow cytometric analysis of MCF7 cells using RIP (D94C12) XP® Rabbit mAb (blue) compared to Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (red).
The 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).
- Meylan, E. and Tschopp, J. (2005) Trends Biochem Sci 30, 151-9.
- Hsu, H. et al. (1996) Immunity 4, 387-96.
- Stanger, B.Z. et al. (1995) Cell 81, 513-23.
- Ting, A.T. et al. (1996) EMBO J 15, 6189-96.
- Kelliher, M.A. et al. (1998) Immunity 8, 297-303.
- Devin, A. et al. (2000) Immunity 12, 419-29.
- Zhang, S.Q. et al. (2000) Immunity 12, 301-11.
- Lin, Y. et al. (1999) Genes Dev 13, 2514-26.
- van Raam, B.J. et al. (2012) Cell Death Differ , . Applications: Western Blotting.
- Salaün, C. et al. (2010) J Biol Chem 285, 34408-18. Applications: Western Blotting.
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For Research Use Only. Not For Use In Diagnostic Procedures.
XP® is a trademark of Cell Signaling Technology, Inc.
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Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.