Product Pathways - NF-kB Signaling
RIP3 (D4G2A) Rabbit mAb #95702
|95702S||100 µl ( 10 western blots )||￥3,250.00||现货查询 购买询价 防伪查询|
|95702||carrier free & custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, F=Flow Cytometry, IF-IC=Immunofluorescence (Immunocytochemistry),
Specificity / Sensitivity
RIP3 (D4G2A) Rabbit mAb 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.
Confocal immunofluorescent analysis of L-929 (left) and Neuro-2a (right) cells using RIP3 (D4G2A) Rabbit mAb (green). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).
Western blot analysis of extracts from various cell lines using RIP3 (D4G2A) Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).
Western blot analysis of extracts from 293T cells, mock transfected (-) or transfected with a construct expressing full-length mouse RIP3 (mRIP3; +) using RIP3 (D4G2A) Rabbit mAb.
Western blot analysis of extracts from wild-type (+) or RIP3 knockout (-) mouse spleen using RIP3 (D4G2A) Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower). Data were kindly provided by Dr. Junying Yuan, Harvard Medical School, Boston MA.
Immunoprecipitation of RIP3 from L-929 cell extracts. Lane 1 is 10% input, lane 2 is Rabbit (DA1E) mAb IgG XP® Isotype Control #3900, and lane 3 is RIP3 (D4G2A) Rabbit mAb. Western blot analysis was performed using RIP3 (D4G2A) Rabbit mAb. A conformation-specific secondary antibody was used to avoid cross reactivity with IgG.
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).
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