RIP3 (E7A7F) XP® Rabbit mAb #10188
- WB
- IP
- IHC
- IF
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 46-62 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| Immunohistochemistry (Paraffin) | 1:50 - 1:200 |
| Immunofluorescence (Immunocytochemistry) | 1:100 - 1:400 |
| Flow Cytometry (Fixed/Permeabilized) | 1:400 - 1:1600 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human RIP3 protein.
Background
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).
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).
- 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.
- Yu, P.W. et al. (1999) Curr Biol 9, 539-42.
- Sun, X. et al. (1999) J Biol Chem 274, 16871-5.
- Zhang, D.W. et al. (2009) Science 325, 332-6.
- He, S. et al. (2009) Cell 137, 1100-11.
- Cho, Y.S. et al. (2009) Cell 137, 1112-23.
- Sun, L. et al. (2012) Cell 148, 213-27.
限制使用
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