FASL antibody (Biotin)

Catalog No. ABIN2689028

Product Details anti-FASL Antibody (Biotin)

Target: FASL (Fas Ligand (TNF Superfamily, Member 6) (FASL))

Reactivity: Mouse

Host: Mouse

Clonality: Monoclonal

Conjugate: This FASL antibody is conjugated to Biotin

Application: Flow Cytometry (FACS), Immunohistochemistry (Formalin-fixed Sections) (IHC (f))

Brand: BD Pharmingen™

Characteristics: The Kay-10 antibody reacts with CD178.1, the Fas Ligand alloantigen (mFasL.1, CD95 Ligand) expressed on activated T lymphocytes of selected strains of mice (eg, C57BL/6, C3H, MRL, NOD, NZB, NZW, and SJL). It does not react with similarly activated T blasts from BALB/c, DBA/1, or DBA/2 mice. It also reacts with Cos cells transfected with mFasL cDNA derived from C57BL/6 and C3H mice, but not with mFasL cDNA from BALB/c or DBA/2 mice. In addition, Kay-10 mAb efficiently blocks cytotoxic activity of a C3H T-cell line, but not a BALB/c T-cell line. Phenotypic and genotypic characterizations of mouse Fas Ligand reveal the existence of two alloantigens: mFasL.1, which is recognized by mAbs Kay-10, MFL3 (Cat. no. 555291), and MFL4 (Cat. no. 555022), and mFasL.2 (recognized by mAbs MFL3 and MFL4). Functional studies suggest that mFasL.2 has higher specific activity than mFasL.1. In the mouse, FasL is expressed on activated T cell lines and in spleen, testis, and eye. FasL mRNA has been demonstrated at various levels in bone marrow, thymus, spleen, lymph node, lung, small intestine, testis, and uterus. Moreover, T-cell activators, but not B-cell activators, enhanced the expression of FasL mRNA in splenocytes, and FasL mRNA was restricted to the T-cell lineage among a panel of cell lines from lymphoid tissues. Fas Ligand is not functional in mice homozygous for the gld(generalized lymphoproliferative disease) mutation, these mice cannot limit the expansion of activated lymphocytes and develop autoimmune disease. Fas Ligand is a member of the TNF/NGF family which binds to CD95 (Fas), inducing apoptotic cell death. This Fas/Fas Ligand interaction is believed to participate in T-cell development, the regulation of immune responses, and cell-mediated cytotoxic mechanisms. There is mounting evidence that Fas Ligand is also pro-inflammatory, mediating neutrophil extravasation and chemotaxis. Fas Ligand is released from the surface of transfectant cells by metalloproteinases, and the soluble Fas Ligand may block the activities of the membrane-bound molecule.

BD Pharmingen™ Biotin Mouse Anti-Mouse CD178.1 - Biotin - Clone KAY-10 - Isotype Mouse IgG2b, κ - Reactivity Ms - 0.5 mg

Purification: The monoclonal antibody was purified from tissue culture supernatant or ascites by affinity chromatography.

Immunogen: Transfected Cell Line

Clone: KAY

Isotype: IgG2b kappa

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

Concentration: 0.5 mg/mL

Buffer: Aqueous buffered solution containing ≤0.09 % sodium azide.

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Handling Advice: The antibody was conjugated with biotin under optimum conditions, and unreacted biotin was removed.

Storage: 4 °C

Storage Comment: Store undiluted at 4°C.

References for anti-FASL antibody (Biotin) (ABIN2689028)

Hohlbaum, Moe, Marshak-Rothstein: "Opposing effects of transmembrane and soluble Fas ligand expression on inflammation and tumor cell survival." in: The Journal of experimental medicine, Vol. 191, Issue 7, pp. 1209-20, (2000) (PubMed).

Pestano, Zhou, Trimble, Daley, Weber, Cantor: "Inactivation of misselected CD8 T cells by CD8 gene methylation and cell death." in: Science (New York, N.Y.), Vol. 284, Issue 5417, pp. 1187-91, (1999) (PubMed).

Schneider, Holler, Bodmer, Hahne, Frei, Fontana, Tschopp: "Conversion of membrane-bound Fas(CD95) ligand to its soluble form is associated with downregulation of its proapoptotic activity and loss of liver toxicity." in: The Journal of experimental medicine, Vol. 187, Issue 8, pp. 1205-13, (1998) (PubMed).

Takeda, Gotoh, Dono, Nishihara, Grochowiecki, Kimura, Yoshida, Ohta, Ota, Ohzato, Umeshita, Takeda, Matsuura, Sakon, Kayagaki, Yagita, Okumura, Miyasaka, Monden: "Protection of islet allografts transplanted together with Fas ligand expressing testicular allografts." in: Diabetologia, Vol. 41, Issue 3, pp. 315-21, (1998) (PubMed).

Kayagaki, Yamaguchi, Nagao, Matsuo, Maeda, Okumura, Yagita: "Polymorphism of murine Fas ligand that affects the biological activity." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 94, Issue 8, pp. 3914-9, (1997) (PubMed).

Griffith, Brunner, Fletcher, Green, Ferguson: "Fas ligand-induced apoptosis as a mechanism of immune privilege." in: Science (New York, N.Y.), Vol. 270, Issue 5239, pp. 1189-92, (1996) (PubMed).

Lau, Yu, Fontana, Stoeckert: "Prevention of islet allograft rejection with engineered myoblasts expressing FasL in mice." in: Science (New York, N.Y.), Vol. 273, Issue 5271, pp. 109-12, (1996) (PubMed).

Lynch, Ramsdell, Alderson: "Fas and FasL in the homeostatic regulation of immune responses." in: Immunology today, Vol. 16, Issue 12, pp. 569-74, (1996) (PubMed).

Bellgrau, Gold, Selawry, Moore, Franzusoff, Duke: "A role for CD95 ligand in preventing graft rejection." in: Nature, Vol. 377, Issue 6550, pp. 630-2, (1995) (PubMed).

Ju, Panka, Cui, Ettinger, el-Khatib, Sherr, Stanger, Marshak-Rothstein: "Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation." in: Nature, Vol. 373, Issue 6513, pp. 444-8, (1995) (PubMed).

Vignaux, Vivier, Malissen, Depraetere, Nagata, Golstein: "TCR/CD3 coupling to Fas-based cytotoxicity." in: The Journal of experimental medicine, Vol. 181, Issue 2, pp. 781-6, (1995) (PubMed).

Brunner, Mogil, LaFace, Yoo, Mahboubi, Echeverri, Martin, Force, Lynch, Ware: "Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas." in: Nature, Vol. 373, Issue 6513, pp. 441-4, (1995) (PubMed).

Smith, Farrah, Goodwin: "The TNF receptor superfamily of cellular and viral proteins: activation, costimulation, and death." in: Cell, Vol. 76, Issue 6, pp. 959-62, (1994) (PubMed).

Takahashi, Tanaka, Brannan, Jenkins, Copeland, Suda, Nagata: "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).

Target Details for FASL

Target: FASL (Fas Ligand (TNF Superfamily, Member 6) (FASL))

Alternative Name: CD178.1 (FASL Products)

Synonyms: ALPS1B antibody, APT1LG1 antibody, APTL antibody, CD178 antibody, CD95-L antibody, CD95L antibody, FASL antibody, TNFSF6 antibody, fasl antibody, Fas-L antibody, Faslg antibody, Tnfsf6 antibody, gld antibody, Apt1Lg1 antibody, Fasl antibody, FASLG antibody, zgc:162027 antibody, Fas ligand antibody, Fas ligand L homeolog antibody, Fas ligand (TNF superfamily, member 6) antibody, FASLG antibody, faslg.L antibody, Fasl antibody, Faslg antibody, faslg antibody

Background: Synonyms: mFasL.1, CD95 Ligand

Pathways: Apoptosis, EGFR Signaling Pathway, Production of Molecular Mediator of Immune Response, Positive Regulation of Endopeptidase Activity