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FLIP Antibody #3210

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Inquiry Info. # 3210

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    Product Specifications

    REACTIVITY H M R Mk
    SENSITIVITY Endogenous
    MW (kDa) 30 FLIP S. 58 FLIP L.
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 
    • Mk-Monkey 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    FLIP Antibody detects endogenous levels of the long and short isoforms of FLIP.

    Species Reactivity:

    Human, Mouse, Rat, Monkey

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding cysteine 155 of FLIP. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    Cellular FLIP (FLICE inhibitory protein) is a regulator of apoptosis that has various names, such as c-FLIP (1), Casper (2), CLARP (3), FLAME (4), I-FLICE (5), MRIT (6), CASH (7), and Usurpin (8). FLIP is expressed as two alternative splice isoforms, FLIP short (FLIPS) and FLIP long (FLIPL). FLIPS contains two death effector domains (DEDs) like those found on the death receptor adaptor protein FADD and the pro-domain of caspase-8. FLIPL shares significant homology with caspase-8 (FLICE), and contains an additional death effector domain, but FLIPL lacks the catalytic active site of the caspases and does not have protease activity. Both FLIP isoforms have been reported to interact with FADD and pro-caspase-8. The role of FLIP in apoptosis is controversial as some research studies have reported it to be anti-apoptotic, while others claim that it is pro-apoptotic. Overexpression of FLIPL can lead to caspase-8 heterodimers that produce an active protease, resulting in apoptosis. However, at physiological levels, it is thought that the binding of FLIP to the DED of FADD results in inhibition of caspase-8 processing. Reduction of FLIP by siRNA or gene targeting sensitizes cells to death receptor-mediated apoptosis. FLIP has also been implicated in the resistance of cancer cells to apoptosis and is upregulated in some cancer types including Hodgkin's lymphoma and ovarian and colon carcinomas (9).

    Alternate Names

    c-FLIP; c-FLIPL; c-FLIPR; c-FLIPS; CASH; CASP8 and FADD like apoptosis regulator; CASP8 and FADD-like apoptosis regulator; CASP8 and FADD-like apoptosis regulator subunit p12; CASP8 and FADD-like apoptosis regulator subunit p43; CASP8AP1; Caspase homolog; Caspase-eight-related protein; Caspase-like apoptosis regulatory protein; caspase-related inducer of apoptosis; Casper; Cellular FLICE-like inhibitory protein; CFLAR; cFLIP; CLARP; FADD-like anti-apoptotic molecule; FADD-like antiapoptotic molecule 1; FLAME; FLAME-1; FLAME1; FLIP; I-FLICE; Inhibitor of FLICE; MACH-related inducer of toxicity; MRIT; testis secretory sperm-binding protein Li 233m; Usurpin; usurpin beta

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