R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
Phospho-RIP (Ser415) (F1U7B) Rabbit mAb #71420
Filter:
- WB
- IP
Supporting Data
| REACTIVITY | H M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 78-82 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
Phospho-RIP (Ser415) (F1U7B) Rabbit mAb recognizes endogenous levels of mouse RIP protein only when phosphorylated at Ser415. This antibody can also detect human RIP protein when phosphorylated at Ser416.
Species Reactivity:
Human, Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser415 of mouse RIP 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).
Phosphorylation of mouse RIP at Ser415 (Ser416 in human) by AMPK in response to metabolic stress can inhibit RIP cell death (9).
Phosphorylation of mouse RIP at Ser415 (Ser416 in human) by AMPK in response to metabolic stress can inhibit RIP cell death (9).
- 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.
- Zhang, T. et al. (2023) Science 380, 1372-1380.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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