AdipoGen Life Sciences

anti-FLIP, mAb (Dave-2)

CHF 495.00
In stock
AG-20B-0005-C100100 µgCHF 495.00
More Information
Product Details
Synonyms I-FLICE; CLARP; CASPER; Usurpin, CASH; FLAME-1
Product Type Monoclonal Antibody
Properties
Clone Dave-2
Isotype Rat IgG2a
Immunogen/Antigen Recombinant human FLIP (aa 1-480).
Application

Immunoprecipitation
Western Blot


Note: Not recommended for immunohistochemistry.

Crossreactivity Human
Mouse
Specificity

Recognizes an epitope (aa 1-200) present in both short (FLIPS) and long (FLIPL) splice variants of human and mouse FLIP.

Concentration 1 mg/ml.
Formulation Liquid. In PBS containing 10% glycerol and 0.02% sodium azide.
Isotype Negative Control

Rat IgG2a Isotype Control

Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Handling Advice Avoid freeze/thaw cycles.
Use/Stability Stable for at least 1 year after receipt when stored at -20°C.
Documents
MSDS Download PDF
Product Specification Sheet
Datasheet Download PDF
Description

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.

Product References
  1. 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 interaction: a new role for Fas ligand in inf: M. Rescigno, et al.; J. Exp. Med. 192, 1661 (2000)
  2. Protein kinase C regulates FADD recruitment and death-inducing signaling complex formation in Fas/CD95-induced apoptosis: M. Gomez-Angelats & J.A. Cidlowski; J. Biol. Chem. 276, 44944 (2001)
  3. NF-kB signals induce the expression of c-FLIP: O. Micheau, et al.; Mol. Cell. Biol. 21, 5299 (2001)
  4. Fas-associated death domain protein (FADD) and caspase-8 mediate up-regulation of c-Fos by Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via a FLICE inhibitory protein (FLIP)-regulated pathway: D. Siegmund, et al.; J. Biol. Chem. 276, 32585 (2001)
  5. Fas aggregation does not correlate with Fas-mediated apoptosis: Y. Lee & E. Shacter; J. Immunol. 167, 82 (2001)
  6. The caspase 8 inhibitor c-FLIP(L) modulates T-cell receptor-induced proliferation but not activation-induced cell death of lymphocytes: S.M. Lens, et al.; Mol. Cell. Biol. 22, 5419 (2002)
  7. Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Signaling in Activated T Cells Abrogates TRAIL-Induced Apoptosis Upstream of the Mitochondrial Amplification Loop and Caspase-8: T.S. Soderstrom, et al.; J. Immunol. 169, 2851 (2002)
  8. Characterization of the human FLICE-inhibitory protein locus and comparison of the anti-apoptotic activity of four different flip isoforms: M. Djerbi, et al.; Scand. J. Immunol. 54, 180 (2002)
  9. c-FLIP efficiently rescues TRAF-2-/- cells from TNF-induced apoptosis: C. Guiet, et al.; Cell Death Differ. 9, 138 (2002)
  10. Expression of the long form of human FLIP by retroviral gene transfer of hemopoietic stem cells exacerbates experimental autoimmune encephalomyelitis: M. Djerbi, et al.; J. Immunol. 170, 2064 (2003)
  11. Chemotherapy enhances TNF-related apoptosis-inducing ligand DISC assembly in HT29 human colon cancer cells: S. Lacour, et al.; Oncogene 22, 1807 (2003)
  12. Bile acids stimulate cFLIP phosphorylation enhancing TRAIL-mediated apoptosis: H. Higuchi, et al.; J. Biol. Chem. 278, 454 (2003)
  13. The anti-apoptotic factor Bcl-2 can functionally substitute for the B cell survival but not for the marginal zone B cell differentiation activity of BAFF: A. Tardivel, et al.; Eur. J. Immunol. 34, 509 (2004)
  14. Targeting Bcl-x(L) in esophageal squamous cancer to sensitize to chemotherapy plus TRAIL-induced apoptosis while normal epithelial cells are protected by blockade of caspase 9: K. Kim, et al.; Cell Death Differ. 11, 583 (2004)
  15. Fas-associated protein with death domain (FADD)-independent recruitment of c-FLIPL to death receptor 5: T.G. Jin, et al.; J. Biol. Chem. 279, 55594 (2004)
  16. The E3 ubiquitin ligase itch couples JNK activation to TNFalpha-induced cell death by inducing c-FLIP(L) turnover: L. Chang, et al.; Cell 124, 601 (2006)
  17. A Protective Role for the Human SMG-1 Kinase against Tumor Necrosis Factor-α-induced Apoptosis: V. Oliveira, et al.; J. Biol. Chem. 283, 13174 (2008)
  18. Cellular FLIP inhibits myeloid cell activation by suppressing selective innate signaling: YJ. Wu, et al.; Reproduction 150, 367 (2015)
  19. Knockdown of RIPK1 markedly exacerbates murine immune-mediated liver injury through massive apoptosis of hepatocytes, independent of necroptosis and inhibition of NF-κB: J. Suda, et al., J. Immunol. 197, 3120 (2016)
  20. The caspase-8 inhibitor emricasan combines with the SMAC mimetic birinapant to induce necroptosis and treat acute myeloid leukemia: G. Brumatti, et al.; Sci. Transl. Med. 8, 339ra69 (2016)
  21. TRAIL receptor gene editing unveils TRAIL-R1 as a master player of apoptosis induced by TRAIL and ER stress: D. Florent, et al.; Oncotarget 8, 9974 (2017)
  22. The Mitochondrial Apoptotic Effectors BAX/BAK Activate Caspase-3 and -7 to Trigger NLRP3 Inflammasome and Caspase-8 Driven IL-1β Activation: J.E. Vince, et al.; Cell Rep. 25, 2339 (2018)
  23. Necroptotic signaling is primed in Mycobacterium tuberculosis-infected macrophages, but its pathophysiological consequence in disease is restricted: M.D. Stutz, et al.; Cell Death Differ. 25, 951 (2018)
  24. Type I interferon signaling mediates Mycobacterium tuberculosis-induced macrophage death: L. Zhang, et al.; J. Exp. Med. 218, e20200887 (2021)
  25. Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis:Y. Tsuchiya, et al.; Nature Commun. 14, 6304 (2023)
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