Cited in 7+ publications.
The Rat Monoclonal anti-FLIP antibody (Clone Dave-2) (ABIN1169019) specifically detects FLIP in WB and IP.
The antibody is reactive with Human and Mouse samples.
Optimal working dilution should be determined by the investigator.
Restrictions
For Research Use only
Format
Liquid
Concentration
Lot specific
Buffer
In PBS containing 10 % glycerol and 0.02 % 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.
Storage
4 °C,-20 °C
Storage Comment
Short Term Storage: +4°C Long Term Storage: -20°C Stable for at least 1 year after receipt when stored at -20°C.
Expiry Date
12 months
Van Opdenbosch, Van Gorp, Verdonckt, Saavedra, de Vasconcelos, Gonçalves, Vande Walle, Demon, Matusiak, Van Hauwermeiren, DHont, Hochepied, Krautwald, Kanneganti, Lamkanfi: "Caspase-1 Engagement and TLR-Induced c-FLIP Expression Suppress ASC/Caspase-8-Dependent Apoptosis by Inflammasome Sensors NLRP1b and NLRC4." in: Cell reports, Vol. 21, Issue 12, pp. 3427-3444, (2018) (PubMed).
Dannappel, Vlantis, Kumari, Polykratis, Kim, Wachsmuth, Eftychi, Lin, Corona, Hermance, Zelic, Kirsch, Basic, Bleich, Kelliher, Pasparakis: "RIPK1 maintains epithelial homeostasis by inhibiting apoptosis and necroptosis." in: Nature, Vol. 513, Issue 7516, pp. 90-4, (2014) (PubMed).
Lens, Kataoka, Fortner, Tinel, Ferrero, MacDonald, Hahne, Beermann, Attinger, Orbea, Budd, Tschopp: "The caspase 8 inhibitor c-FLIP(L) modulates T-cell receptor-induced proliferation but not activation-induced cell death of lymphocytes." in: Molecular and cellular biology, Vol. 22, Issue 15, pp. 5419-33, (2002) (PubMed).
Gómez-Angelats, Cidlowski: "Protein kinase C regulates FADD recruitment and death-inducing signaling complex formation in Fas/CD95-induced apoptosis." in: The Journal of biological chemistry, Vol. 276, Issue 48, pp. 44944-52, (2001) (PubMed).
Micheau, Lens, Gaide, Alevizopoulos, Tschopp: "NF-kappaB signals induce the expression of c-FLIP." in: Molecular and cellular biology, Vol. 21, Issue 16, pp. 5299-305, (2001) (PubMed).
Djerbi, Darreh-Shori, Zhivotovsky, Grandien: "Characterization of the human FLICE-inhibitory protein locus and comparison of the anti-apoptotic activity of four different flip isoforms." in: Scandinavian journal of immunology, Vol. 54, Issue 1-2, pp. 180-9, (2001) (PubMed).
Rescigno, Piguet, Valzasina, Lens, Zubler, French, Kindler, Tschopp, Ricciardi-Castagnoli et al.: "Fas engagement induces the maturation of dendritic cells (DCs), the release of interleukin (IL)-1beta, and the production of interferon gamma in the absence of IL-12 during DC-T cell cognate ..." in: The Journal of experimental medicine, Vol. 192, Issue 11, pp. 1661-8, (2000) (PubMed).
Target
FLIP (CFLAR)
(CASP8 and FADD-Like Apoptosis Regulator (CFLAR))
Alternative Name
FLIP
Background
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.