R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
RIP3 (E1Y9Z) Rabbit mAb (BSA and Azide Free) #91171
Filter:
- ELISA
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Rabbit IgG |
Application Key:
- ELISA-ELISA
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.
BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.
Formulation
Supplied in 1X PBS (10 mM Na2HPO4, 3 mM KCl, 2 mM KH2PO4, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.
Storage
Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.
Specificity / Sensitivity
RIP3 (E1Y9Z) Rabbit mAb (BSA and Azide Free) detects endogenous levels of RIP3.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with synthetic peptide corresponding to residues in human RIP3.
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).
- 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.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意，否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件，除非书 CST 的合法授书代表以书面形式书独接受， 否书均被拒书，并且无效。
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For Research Use Only. Not For Use In Diagnostic Procedures.
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