FLIP Antikörper (AA 1-480)

Produktnummer ABIN1169018

Es sind 9+ Publikationen für dieses Produkt verfügbar. Der Maus Monoklonal anti-FLIP Antikörper wird verwendet zum Nachweis von FLIP in Proben von Human. Er wurde validiert für WB, IHC und ICC.

Kurzübersicht für FLIP Antikörper (AA 1-480) (ABIN1169018)

Target: FLIP (CFLAR) (CASP8 and FADD-Like Apoptosis Regulator (CFLAR))

Reaktivität: Human

Wirt: Maus

Klonalität: Monoklonal

Konjugat: Dieser FLIP Antikörper ist unkonjugiert

Applikation: Western Blotting (WB), Immunohistochemistry (IHC), Immunocytochemistry (ICC)

Klon: NF6

Produktdetails anti-FLIP Antikörper

Bindungsspezifität: AA 1-480

Spezifität: Recognizes short (FLIPS) and long (FLIPL) splice variants of human FLIP. This antibody recognizes an epitope in the N-terminal DED region (aa1-194).

Kreuzreaktivität: Human

Aufreinigung: Purified from concentrated hybridoma tissue culture supernatant.

Immunogen: Recombinant human FLIP (aa 1-480).

Isotyp: IgG1

Anwendungsinformationen

Applikationshinweise: Optimal working dilution should be determined by the investigator.

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Konzentration: Lot specific

Buffer: In PBS containing 10 % glycerol and 0.02 % sodium azide.

Konservierungsmittel: Sodium azide

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

Lagerung: 4 °C,-20 °C

Informationen zur Lagerung: Short Term Storage: +4°C
Long Term Storage: -20°C
Stable for at least 1 year after receipt when stored at -20°C.

Haltbarkeit: 12 months

Referenzen für anti-FLIP Antikörper (ABIN1169018)

Hartwig, Montinaro, von Karstedt, Sevko, Surinova, Chakravarthy, Taraborrelli, Draber, Lafont, Arce Vargas, El-Bahrawy, Quezada, Walczak: "The TRAIL-Induced Cancer Secretome Promotes a Tumor-Supportive Immune Microenvironment via CCR2." in: Molecular cell, Vol. 65, Issue 4, pp. 730-742.e5, (2017) (PubMed).

Golks, Brenner, Krammer, Lavrik: "The c-FLIP-NH2 terminus (p22-FLIP) induces NF-kappaB activation." in: The Journal of experimental medicine, Vol. 203, Issue 5, pp. 1295-305, (2006) (PubMed).

Eichhorst, Krueger, Müerköster, Fas, Golks, Gruetzner, Schubert, Opelz, Bilzer, Gerbes, Krammer: "Suramin inhibits death receptor-induced apoptosis in vitro and fulminant apoptotic liver damage in mice." in: Nature medicine, Vol. 10, Issue 6, pp. 602-9, (2004) (PubMed).

Jang, Krammer, Salgame: "Lack of proapoptotic activity of soluble CD95 ligand is due to its failure to induce CD95 oligomers." in: Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, Vol. 23, Issue 8, pp. 441-7, (2003) (PubMed).

Leverkus, Sprick, Wachter, Mengling, Baumann, Serfling, Bröcker, Goebeler, Neumann, Walczak: "Proteasome inhibition results in TRAIL sensitization of primary keratinocytes by removing the resistance-mediating block of effector caspase maturation." in: Molecular and cellular biology, Vol. 23, Issue 3, pp. 777-90, (2003) (PubMed).

Kim, Suh, Sporn, Reed: "An inducible pathway for degradation of FLIP protein sensitizes tumor cells to TRAIL-induced apoptosis." in: The Journal of biological chemistry, Vol. 277, Issue 25, pp. 22320-9, (2002) (PubMed).

Frese, Brunner, Gugger, Uduehi, Schmid et al.: "Enhancement of Apo2L/TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)-induced apoptosis in non-small cell lung cancer cell lines by chemotherapeutic agents without correlation to the ..." in: The Journal of thoracic and cardiovascular surgery, Vol. 123, Issue 1, pp. 168-74, (2002) (PubMed).

Sprick, Rieser, Stahl, Grosse-Wilde, Weigand, Walczak: "Caspase-10 is recruited to and activated at the native TRAIL and CD95 death-inducing signalling complexes in a FADD-dependent manner but can not functionally substitute caspase-8." in: The EMBO journal, Vol. 21, Issue 17, pp. 4520-30, (2002) (PubMed).

Scaffidi, Schmitz, Krammer, Peter: "The role of c-FLIP in modulation of CD95-induced apoptosis." in: The Journal of biological chemistry, Vol. 274, Issue 3, pp. 1541-8, (1999) (PubMed).

Details zu FLIP

Target: FLIP (CFLAR) (CASP8 and FADD-Like Apoptosis Regulator (CFLAR))

Andere Bezeichnung: FLIP

Hintergrund: FLIP is an apoptosis regulator protein which functions as a crucial link between cell survival and cell death pathways in mammalian cells and acts as an inhibitor of TNFRSF6 mediated apoptosis. A proteolytic fragment (p43) is likely retained in the death-inducing signaling complex (DISC) thereby blocking further recruitment and processing of caspase-8 at the complex. Full length and shorter isoforms have been shown either to induce apoptosis or to reduce TNFRSF-triggered apoptosis. FLIP lacks enzymatic (caspase) activity. FLIP is highly expressed in skeletal muscle, pancreas, heart, kidney, placenta and peripheral blood leukocytes.

UniProt: O15519

Pathways: Apoptose, Regulation of Muscle Cell Differentiation, Skeletal Muscle Fiber Development