FASL Antikörper

Produktnummer ABIN1176981

Dieses Anti-FASL-Antikörper ist ein Armenischer Hamster Monoklonal-Antikörper zur Detektion von FASL in FACS und BR. Geeignet für Maus. Dieses Primary Antibody wurde in 17+ Publikationen zitiert.

Kurzübersicht für FASL Antikörper (ABIN1176981)

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

Reaktivität: Maus

Wirt: Armenischer Hamster

Klonalität: Monoklonal

Konjugat: Dieser FASL Antikörper ist unkonjugiert

Applikation: Flow Cytometry (FACS), Blocking Reagent (BR)

Klon: MFL3

Produktdetails anti-FASL Antikörper

Marke: BD Pharmingen™

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

Sterilität: 0.2 μm filtered

Endotoxin-Niveau: Endotoxin level is ≤ 0.01 EU/μg (≤ 0.001 ng/μg) of protein as determined by the LAL assay.

Immunogen: Mouse FasL-transfected cells

Isotyp: IgG1 kappa

Anwendungsinformationen

Applikationshinweise: Enriched splenic T cells can be induced to express Fas Ligand by 6-8-hour culture with plate-bound anti-mouse CD3 mAb 17A2 (Cat. No. 555273), mAb 145-2C11 (Cat. No. 557306), or mAb 500A2 (Cat. No. 553238). Because Fas Ligand is expressed at low density on activated cells, it may be desirable to amplify staining by using a biotinylated second-step antibody with a bright third-step reagent, such as PE Streptavidin (Cat. No. 554061). The BD Biosciences anti-hamster IgG mAb cocktails, either biotin- or PE-conjugated (Cat. No. 554010 or 554056, respectively) are not effective for staining with mAb MFL3. Other reported applications include blocking of the cytotoxic activities of the mouse FasLigand-transfected L5178Y T lymphoma and influenza-specific CD8+ BALB/c CTL clones.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: 1.0 mg/mL

Buffer: No azide/low endotoxin: Aqueous buffered solution containing no preservative, 0.2μm sterile filtered.

Konservierungsmittel: Azide free

Lagerung: 4 °C

Informationen zur Lagerung: Store undiluted at 4°C. This preparation contains no preservatives, thus it should be handled under aseptic conditions.

Referenzen für anti-FASL Antikörper (ABIN1176981)

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).

Fuller, Ravichandran, Braciale: "Phosphatidylinositol 3-kinase-dependent and -independent cytolytic effector functions." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 162, Issue 11, pp. 6337-40, (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).

Griffith, Ferguson: "The role of FasL-induced apoptosis in immune privilege." in: Immunology today, Vol. 18, Issue 5, pp. 240-4, (1997) (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).

Kojima, Shinohara, Hanaoka, Someya-Shirota, Takagaki, Ohno, Saito, Katayama, Yagita, Okumura: "Two distinct pathways of specific killing revealed by perforin mutant cytotoxic T lymphocytes." in: Immunity, Vol. 1, Issue 5, pp. 357-64, (1995) (PubMed).

Ramsdell, Seaman, Miller, Picha, Kennedy, Lynch: "Differential ability of Th1 and Th2 T cells to express Fas ligand and to undergo activation-induced cell death." in: International immunology, Vol. 6, Issue 10, pp. 1545-53, (1995) (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).

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).

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).

Suda, Okazaki, Naito, Yokota, Arai, Ozaki, Nakao, Nagata: "Expression of the Fas ligand in cells of T cell lineage." in: Journal of immunology (Baltimore, Md. : 1950), Vol. 154, Issue 8, pp. 3806-13, (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).

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).

Details zu FASL

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

Andere Bezeichnung: CD178

Hintergrund: The MFL3 antibody reacts with CD178 (Fas Ligand, CD95 Ligand) on all strains tested. In the mouse, Fas Ligand 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 lympho-proliferative 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 proinflammatory, 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. The MFL3 mAb has been reported to efficiently inhibit the cytotoxicity of mouse Fas Ligand-transfected cells against human Fas-transfected cells. This hamster mAb to a mouse leukocyte antigen does not cross-react with rat leukocytes.
Synonyms: Fas Ligand, CD95 Ligand

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