Fas Ligand (TNF Superfamily, Member 6) (FASL) antibody
Alternatives Western Blotting (WB), Immunohistochemistry (Frozen Sections) (IHC (fro)), Immunoprecipitation (IP)
|7 references available|
|Quantity||0.1 mg (0.5 mg/ml)|
|Price||Product not available in this region.|
|Immunogen||Recombinant Human FasL|
Fas (APO-1, CD95) is a 45 kD cell surface protein that mediates apoptosis when crosslinked with agonistic anti-Fas antibodies or Fas ligand (FasL). Fas belongs to the TNF (tumor necrosis factor)/NGF (nerve growth factor) receptor family, and is expressed in various tissue and cells including the thymus, liver, ovary and lung. FasL is a member of the TNF cytokine family that induces apoptosis by binding to Fas, its cell-surface receptor. FasL may exist in both membrane and soluble forms and expressed on activated T cells, NK cells, and other immunologically privileged” sites. Both Fas and FasL are thought to play an important role in the apoptotic processes that take place during T cell development.
G247-4 recognizes human FasL. It recognizes both the membrane bound (FasL) and soluble (sFasL) forms. A recombinant protein containing the external domain of human FasL was used as immunogen. FasL and sFasL migrate at reduced molecular weights of 40 and 26 kD, respectively. However, the molecular weights observed in a particular sample may vary according to FasL and sFasL glycosylation and breakdown patterns as described in Tanaka et al. For example, FasL may migrate as a doublet of 40 and 42 kD.
Synonyms: Fas Ligand, CD95 Ligand
1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
|Molecular Weight||42 kDa, 40 kDa (membrane), 26 kDa (soluble)|
Related Products: ABIN967389
|Synonyms||FASL, CD178, CD95L, TNFSF6, APT1LG1, gld, Fas-L, Faslg, Tnfsf6, Fas-Ligand, FASLG, fasl, APT1, CD95, FAS1, APO-1, FASTM, ALPS1A, TNFRSF6, lpr, APO1, TNFR6, Tnfrsf6, AI196731, Fasl, CD95-L, Apt1Lg1, FAS, LOC574159, zgc:162027|
|Application Notes||Applications include immunoprecipitation (1-2 µg/ml), western blot analysis (1-2 µg/ml) and immunohistochemical staining of acetone-fixed frozen tissue sections (0.5-4 µg/ml). G247-4 is not recommended for flow cytometry. For flow cytometry application, clone NOK-1 (purified, or biotin-conjugated) is recommended.|
|Purification||Purified from tissue culture supernatant or ascites by affinity chromatography.|
|Buffer||Aqueous buffered solution.|
|Preservative||0.09% Sodium azide.|
|Storage||Store undiluted at 4°C.|
|Restrictions||For Research Use only|
Kayagaki, Kawasaki, Ebata et al.: "Metalloproteinase-mediated release of human Fas ligand." in: The Journal of experimental medicine, Vol. 182, Issue 6, pp. 1777-83, 1996 (PubMed).
Takahashi, Tanaka, Brannan et al.: "Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand." in: Cell, Vol. 76, Issue 6, pp. 969-76, 1994 (PubMed).
Tanaka, Suda, Takahashi et al.: "Expression of the functional soluble form of human fas ligand in activated lymphocytes." in: The EMBO journal, Vol. 14, Issue 6, pp. 1129-35, 1995 (PubMed).
Griffith, Ferguson: "The role of FasL-induced apoptosis in immune privilege." in: Immunology today, Vol. 18, Issue 5, pp. 240-4, 1997 (PubMed).
Sträter, Wellisch, Riedl et al.: "CD95 (APO-1/Fas)-mediated apoptosis in colon epithelial cells: a possible role in ulcerative colitis." in: Gastroenterology, Vol. 113, Issue 1, pp. 160-7, 1997 (PubMed).
Orlinick, Vaishnaw, Elkon et al.: "Requirement of cysteine-rich repeats of the Fas receptor for binding by the Fas ligand." in: The Journal of biological chemistry, Vol. 272, Issue 46, pp. 28889-94, 1997 (PubMed).
Orlinick, Elkon, Chao: "Separate domains of the human fas ligand dictate self-association and receptor binding." in: The Journal of biological chemistry, Vol. 272, Issue 51, pp. 32221-9, 1998 (PubMed).