Abcam, ab6144, Anti-FLIP antibody

Size: 100µg
Rabbit Polyclonal FLIP antibody. Suitable for WB, ICC/IF and reacts with Human samples. Cited in 8 publications. Immunogen corresponding to Synthetic Peptide within Human CFLAR aa 400 to C-terminus.
Key facts
Host species:Rabbit,
Clonality:Polyclonal,
Isotype:IgG,
Carrier free:No,
Reacts with:Human,
Applications:ICC/IF, WBSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Immunogen:Synthetic Peptide within Human CFLAR aa 400 to C-terminus. The exact immunogen used to generate this antibody is proprietary information.O15519

Properties and Storage Information:
Form-Liquid, Purification technique-Affinity purification, Purification notes-Purified IgG prepared by ion exchange chromatography., Storage buffer-pH: 7.2Preservative: 0.02% Sodium azideConstituents: PBS, Shipped at conditions-Blue Ice, Appropriate short-term storage duration-1-2 weeks, Appropriate short-term storage conditions-+4°C, Appropriate long-term storage conditions--20°C, Aliquoting information-Upon delivery aliquot, Storage information-Avoid freeze / thaw cycle

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
FLIP also known as c-FLIP or CASP8 and FADD-like apoptosis regulator is an important protein that inhibits apoptosis. It has a molecular mass of around 55-58 kDa and comes in multiple isoforms including c-FLIP(L) and c-FLIP(S). FLIP is expressed in many tissues such as the thymus spleen and lungs and plays a role in immune regulation by modulating apoptosis induced by death receptors like Fas and TNFR1. Its regulation of cell death makes it key to cell survival especially in the context of immune cells.
Biological function summary
FLIP protein impacts cellular processes by blocking the activation of caspase-8 preventing the apoptosis cascade from proceeding. It is not typically part of a large complex but interacts directly with the death-inducing signaling complex (DISC). By inhibiting the apoptotic machinery it protects cells from unnecessary death signals facilitating controlled cellular turnover and immune responses.
Pathways
FLIP affects apoptosis and NF-kB signaling. These pathways are vital for cell survival inflammation and immune responses. FLIP interacts closely with Fas-associated protein with death domain (FADD) and caspase-8 to regulate apoptotic pathways. It acts as a checkpoint in intrinsic and extrinsic apoptosis pathways thereby influencing both normal and pathological processes such as immune cell survival and proliferation.
FLIP expression connects to cancer and autoimmune disorders. Its overexpression can contribute to cancer progression by allowing cancer cells to escape apoptosis leading to uncontrolled cell growth. Furthermore it can be linked to autoimmune disorders where inappropriate control of apoptosis results in prolonged survival of autoreactive immune cells. In these contexts FLIP’s interaction with proteins such as Fas and TNFR1 becomes significant highlighting its potential as a therapeutic target in mitigating these diseases.