Product Pathways - Apoptosis
Fas (C18C12) Rabbit mAb #4233
|W IHC-P||H||Endogenous||40-50||Rabbit IgG|
Reactivity Key: H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
Fas (C18C12) Rabbit mAb detects endogenous levels of total human Fas protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys259 of human Fas, within the intracellular region.
Western blot analysis of extracts from COS cells, mock transfected or transfected with human Fas, and from ACHN and HT-1080 cell lines using Fas (C18C12) Rabbit mAb.
Immunohistochemical analysis of paraffin-embedded human colon carcinoma using Fas (C18C12) Rabbit mAb.
Immunohistochemical analysis of paraffn embedded human colon using Fas (C18C12) Rabbit mAb in the presence of control peptide (left) or antigen specific peptide (right).
Association of the receptor Fas with its ligand FasL triggers an apoptotic pathway that plays an important role in immune regulation, development, and progression of cancers (1,2). Loss of function mutation in either Fas (lpr mice) or FasL (gld mice) leads to lymphadenopathy and splenomegaly as a result of decreased apoptosis in CD4-CD8- T lymphocytes (3,4). FasL (CD95L, Apo-1L) is a type II transmembrane protein of 280 amino acids (runs at approximately 40 kDa upon glycosylation) that belongs to the TNF family, which also includes TNF-α, TRAIL, and TWEAK. Binding of FasL to its receptor triggers the formation of a death-inducing signaling complex (DISC) involving the recruitment of the adaptor protein FADD and caspase-8 (5). Activation of caspase-8 from this complex initiates a caspase cascade resulting in the activation of caspase-3 and subsequent cleavage of proteins leading to apoptosis. Unlike Fas, which is constitutively expressed by various cell types, FasL is predominantly expressed on activated T lymphocytes, NK cells, and at immune privileged sites (6). FasL is also expressed in several tumor types as a mechanism to evade immune surveillance (7). Similar to other members of the TNF family, FasL can be cleaved by metalloproteinases producing a 26 kDa trimeric soluble form (8,9).
- Suda, T. et al. (1993) Cell 75, 1169-78.
- Lee, H.O. and Ferguson, T.A. (2003) Cytokine Growth Factor Rev 14, 325-35.
- Watanabe-Fukunaga, R. et al. (1992) Nature 356, 314-7.
- Hahne, M. et al. (1995) Int Immunol 7, 1381-6.
- Nagata, S. (1997) Cell 88, 355-65.
- Green, D.R. and Ferguson, T.A. (2001) Nat Rev Mol Cell Biol 2, 917-24.
- Walker, P.R. et al. (1997) J Immunol 158, 4521-4.
- Kayagaki, N. et al. (1995) J Exp Med 182, 1777-83.
- Tanaka, M. et al. (1995) EMBO J 14, 1129-35.
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For Research Use Only. Not For Use In Diagnostic Procedures.