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  3. Phospho-RIP (Ser321) (E9K2A) Rabbit mAb
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Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Phospho-RIP (Ser321) (E9K2A) Rabbit mAb #38662

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  • WB
  • IF
  • F
Western blot analysis of extracts from C2C12 cells, untreated (-) or treated with Mouse Tumor Necrosis Factor-α (mTNF-α) #5178 (20 ng/ml; indicated times), using Phospho-RIP (Ser321) (E9K2A) Rabbit mAb (upper), total RIP (D94C12) XP® Rabbit mAb #3493 (middle), or GAPDH (D16H11) XP® Rabbit mAb #5174 (lower).
1/5

To Purchase # 38662

Cat. #

Size

Price

Inventory

38662T
20 µl
¥1,570

库存紧张

38662S
100 µl
¥5,220

库存充足

Supporting Data

REACTIVITY M
SENSITIVITY Endogenous
MW (kDa) 78
Source/Isotype Rabbit IgG
Application Key:
  • WB-Western Blotting 
  • IF-Immunofluorescence 
  • F-Flow Cytometry 
Species Cross-Reactivity Key:
  • M-Mouse 
  • Related Products

Product Information

Product Usage Information

Application Dilution
Western Blotting 1:1000
Immunofluorescence (Immunocytochemistry) 1:400 - 1:800
Flow Cytometry (Fixed/Permeabilized) 1:400 - 1:1600

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.

For a carrier free (BSA and azide free) version of this product see product #33527.

Protocol

Specificity / Sensitivity

Phospho-RIP (Ser321) (E9K2A) Rabbit mAb recognizes endogenous levels of mouse RIP protein only when phosphorylated at Ser321.

Species Reactivity:

Mouse

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser321 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).
Necroptosis, a regulated pathway for necrotic cell death, is triggered by a number of inflammatory signals, including cytokines in the tumor necrosis factor (TNF) family, pathogen sensors such as toll-like receptors (TLRs), and ischemic injury (9,10). The process is negatively regulated by caspases and is initiated through a complex containing the RIP and RIP3 kinases, typically referred to as the necrosome. Necroptosis is inhibited by a small molecule inhibitor of RIP, necrostatin-1 (Nec-1) (11). Research studies show that necroptosis contributes to a number of pathological conditions, and Nec-1 has been shown to provide neuroprotection in models such as ischemic brain injury (12). RIP is phosphorylated at several sites within the kinase domain that are sensitive to Nec-1, including Ser14, Ser15, Ser161, and Ser166 (13).

RIP is also phosphorylated at Ser321(mouse)/Ser320(human) by MAPKAPK-2 (MK-2) and TAK1 in response to inflammatory signals such as TNF-α and LPS (14-17). Phosphorylation at this site suppresses RIP mediated apoptosis by inhibiting its interaction with FADD and caspase-8 (14-17).
  1. Meylan, E. and Tschopp, J. (2005) Trends Biochem Sci 30, 151-9.
  2. Hsu, H. et al. (1996) Immunity 4, 387-96.
  3. Stanger, B.Z. et al. (1995) Cell 81, 513-23.
  4. Ting, A.T. et al. (1996) EMBO J 15, 6189-96.
  5. Kelliher, M.A. et al. (1998) Immunity 8, 297-303.
  6. Devin, A. et al. (2000) Immunity 12, 419-29.
  7. Zhang, S.Q. et al. (2000) Immunity 12, 301-11.
  8. Lin, Y. et al. (1999) Genes Dev 13, 2514-26.
  9. Christofferson, D.E. and Yuan, J. (2010) Curr Opin Cell Biol 22, 263-8.
  10. Kaczmarek, A. et al. (2013) Immunity 38, 209-23.
  11. Degterev, A. et al. (2008) Nat Chem Biol 4, 313-21.
  12. Degterev, A. et al. (2005) Nat Chem Biol 1, 112-9.
  13. Ofengeim, D. and Yuan, J. (2013) Nat Rev Mol Cell Biol 14, 727-36.
  14. Jaco, I. et al. (2017) Mol Cell 66, 698-710.e5.
  15. Geng, J. et al. (2017) Nat Commun 8, 359.
  16. Dondelinger, Y. et al. (2017) Nat Cell Biol 19, 1237-47.
  17. Menon, M.B. et al. (2017) Nat Cell Biol 19, 1248-59.

Database Links

UniProt ID: Q60855


Entrez-Gene Id: 19766


限制使用

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