Cell Signaling Technology

Product Pathways - NF-kB Signaling

RIP3 (D4G2A) Rabbit mAb (PE Conjugate) #48006

No. Size Price
48006S 100 µl ( 50 tests ) ¥3,986.00 现货查询 购买询价
48006 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
F 1:50 Mouse, Endogenous Rabbit IgG
CS-CA 1:50

Species cross-reactivity is determined by western blot.

Applications Key: F=Flow Cytometry, CS-CA=CellSimple Cell-Assay,

Specificity / Sensitivity

RIP3 (D4G2A) Rabbit mAb (PE Conjugate) recognizes endogenous levels of total RIP3 protein from mouse.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val370 of mouse RIP3 protein.

Description

This Cell Signaling Technology antibody is conjugated to phycoerythrin (PE) and tested in-house for direct flow cytometry and CellSimple™ cell-assay analysis in mouse cells. This antibody is expected to exhibit the same species cross-reactivity as the unconjugated RIP3 (D4G2A) Rabbit mAb #95702.

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of Neuro-2a (blue) and L-929 (green) cells using RIP3 (D4G2A) Rabbit mAb (PE Conjugate).

Cell-based assay

Cell-based assay

CellSimple™ cell-based analysis of Neuro-2a (blue) and L-929 (grey) cells using RIP3 (D4G2A) Rabbit mAb (PE Conjugate).

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).

  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.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.

CellSimple is a trademark of Cell Signaling Technology, Inc.

Cell Signaling Technology® is a trademark of Cell Signaling Technology, Inc.

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