epitope corresponding to phosphorylated Ser 191 of FADD of mouse origin
Modification
Phosphoralated
Modification Notes
In contrast to growth factors which promote cell proliferation, FAS ligand (FAS-L) and tumor necrosis factor (TNF) rapidly induce apoptosis. Cellular response to FAS-L and TNF is mediated by structurally related receptors containing a conserved “death domain” and belonging to the TNF receptor superfamily. TRADD, FADD and RIP are FAS/TNF-RI interacting proteins that contain a death domain homologous region (DDH). TRADD (TNF-RI-associated death domain) and FADD (FAS-associated death domain) are proteins that associate with the death domains of both FAS and TNF-RI via their DDH regions. Overexpression of TRADD leads to NFkB activation and apoptosis in the absence of TNF. Overexpression of FADD causes apoptosis, which can be blocked by the cow pox protein CrmA, suggesting that FADD lies upstream of ICE and possibly other serine proteases. The receptor interacting protein, RIP, associates with FAS exclusively via its DDH, and this association is abrogated in lpr mutants. Unlike TRADD and FADD, RIP contains a putative amino terminal kinase domain.
Key Feature
Clonality
Polyclonal
Isotype
IgG
Host Species
Rabbit
Tested Applications
WBIPIFELISA
recommended for detection of Ser 191 phosphorylated FADD of mouse and, to a lesser extent, human origin by WB, IP, IF and ELISA:
Species Reactivity
HumanMouseRat
Concentration
1mg/ml
Purification
Affinity purified
Target Information
Alternative Names
epitope corresponding to phosphorylated Ser 191 of FADD of mouse origin
Tissue Specificity
epitope corresponding to phosphorylated Ser 191 of FADD of mouse origin