SpecificityPhospho-RIP3 ( S316 ) Antibody detects endogenous levels of RIP3 only when phosphorylated at S316
Immunogen TypePeptide-KLH
Immunogen DescriptionA synthesized peptide derived from human RIP3 (Phospho- Ser316 )
Alternative NamesReceptor interacting protein 3 antibody
Receptor interacting serine threonine kinase 3 antibody
Receptor interacting serine threonine protein kinase 3 antibody
Receptor-interacting protein 3 antibody
Receptor-interacting serine threonine-protein kinase 3 antibody
RIP 3 antibody
RIP like protein kinase 3 antibody
RIP-3 antibody
RIP-like protein kinase 3 antibody
RIPK 3 antibody
RIPK3 antibody
RIPK3_HUMAN antibody
Accession No.Swiss-Prot#:Q9QZL0 NCBI Gene ID56532
Calculated MW46-62
Concentration1.0mg mL
FormulationRabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+) pH 7.4 150mM NaCl 0.02% sodium azide and 50% glycerol.
StorageStore at -20˚C
Application Details
WB dilution:1:1000
Images
Western blot analysis RIP3 (Phospho- Ser316 ) using EGF treated MCF7 whole cell lysates
Product Description
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-��B, 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-��B 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 I��B phosphorylation and degradation (6,7). Overexpression of RIP induces both NF-��B activation and apoptosis (2,3). Caspase-8-dependent cleavage of the RIP death domain can trigger the apoptotic activity of RIP (8)
Yes
