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The (fli:GFP) Casper zebrafish embryo can be used as an efficient animal model to study metastatic behavior of human CM cells and warrants further testing of drug efficacy to aid care of CM patients.
Inhibition of BET bromodomain-dependent XIAP and FLIP expression sensitizes KRAS-mutated non-small cell lung cancer to pro-apoptotic agents.
the c-FLIP and NOXA (show PMAIP1 Proteins)/Mcl-1 (show MCL1 Proteins) axis participated in the synergistic effect of pemetrexed plus cisplatin in human choroidal melanoma cells
The strongest interaction result in relation to overall breast cancer risk was found between CFLAR-rs7558475 and current smoking (ORint = 0.77, 95% CI: 0.67-0.88, pint = 1.8 x 10(-4) ). The interaction with the strongest statistical evidence was found between 5q14-rs7707921 and alcohol consumption (ORint =1.36, 95% CI: 1.16-1.59, pint = 1.9 x 10(-5) ) in relation to ER- disease risk
findings suggest that expression of cFLIPL regulates the basal interaction of Bcl-2 (show BCL2 Proteins) with Beclin-1 (show BECN1 Proteins) and substantiates p53 (show TP53 Proteins) dependent ubiquitination of Beclin-1 (show BECN1 Proteins) during autophagic stress to determine the fate of cell death or survival.
Using the tDED filament structure as a template, structural analyses reveal the interaction surfaces between FADD (show FADD Proteins) and caspase-8 (show CASP8 Proteins) and the distinct mechanisms of regulation by cFLIP and MC159 through comingling and capping, respectively.
Data in this study show that cFLIPL inhibits IFN regulatory factor 3 (IRF3 (show IRF3 Proteins)), a transcription factor central for IFN-beta (show IFNB1 Proteins) and IFN-stimulated gene expression.
CFLAR levels were substantially decreased in the livers of subjects with NAFLD and NASH, as compared to that in nonsteatotic controls.
association of c-FLIPL and TIP49 provided an additional mechanism involved in c-FLIPL-mediated functions, including Wnt (show WNT2 Proteins) activation
CFLAR role in the necroptosis in fibroblasts
c-FLIP modulation of AKT activity is crucial in controlling PERK signalling and sensitivity to endoplasmic reticulum stress.
Regulatory T cells have a high apoptosis rate ex vivo correlating with low c-FLIP expression.
In conclusion, our data indicated that miR-150 potentially contributes to the hepatic steatosis and insulin resistance in NAFLD. miR-150/CFLAR pathway may be a new therapeutic strategy against NAFLD.
Findings establish CFLAR as a key suppressor of steatohepatitis and indicate that the development of CFLAR-peptide-mimicking drugs and the screening of small-molecular inhibitors that specifically block ASK1 (show MAP3K5 Proteins) dimerization are new and feasible approaches for NASH (show SAMSN1 Proteins) treatment.
knockdown of cFLIPL and induced expression of FADD (show FADD Proteins) rapidly accumulate intracellular ROS (show ROS1 Proteins) accompanied by JNK1 (show MAPK8 Proteins) activation to substantiate apoptosis.
CASP8 (show CASP8 Proteins) is present exclusively as its cleaved p43 (show AIMP1 Proteins) product, bound to cFLIPL.
The generation of mouse line with Flip deficiency in cells that express cre under the CD11c (show ITGAX Proteins) promoter is reported.
c-FLIPL deficiency induces the caspase (show CASP3 Proteins)-mediated processing of RTN4 (show RTN4 Proteins), thus affecting endoplasmic reticulum (ER) shape and coupling to mitochondria. Thus, it was concluded that c-FLIPL is a novel regulator of ER morphology and ER-mitochondria crosstalk.
Acute organ failure following the loss of anti-apoptotic cellular FLICE-inhibitory protein involves activation of innate immune receptors.
The results reveal a novel inhibitory role of c-FLIP in myeloid cell activation and demonstrate the unexpected anti-inflammatory activity of c-FLIP.
results indicate downregulation of cFLIP during structural luteal regression, suggesting that cFLIP plays a survival role in the bovine corpus luteum
Conservation of FLIP's ability to inhibit apoptosis and to downregulate NF-kappaB (show NFKB1 Proteins) activation across species.
cellular-Flice like inhibitory protein (cFLIP) long form, plays an anti-apoptotic role in the granulosa cells of healthy follicles of pig ovaries [cFLIP]
Intracellular remodeling with overexpression of pig c (show PIGC Proteins)-FLIP in xenograft cells may decrease the innate cellular responses against xenografts, facilitating long-term xenograft survival.
Intracellular remodeling with the overexpression of c-FLIP(S/L) in xenograft cells may avoid innate cellular attacks against xenografts and facilitate long-term xenograft survival.
Overexpression of c-FLIP in xenograft cells may prevent innate cellular attacks against xenografts opening the window of opportunity for long-term xenograft survival.
The protein encoded by this gene is a regulator of apoptosis and is structurally similar to caspase-8. However, the encoded protein lacks caspase activity and appears to be itself cleaved into two peptides by caspase-8. Several transcript variants encoding different isoforms have been found for this gene, and partial evidence for several more variants exists.
, CASP8 and FADD-like apoptosis regulator
, flice/caspase-i inhibitory protein
, cellular FLICE-like inhibitory protein
, CASP8 and FADD-like apoptosis regulator-like
, FADD-like anti-apoptotic molecule
, FADD-like antiapoptotic molecule 1
, MACH-related inducer of toxicity
, caspase homolog
, caspase-eight-related protein
, caspase-like apoptosis regulatory protein
, caspase-related inducer of apoptosis
, inhibitor of FLICE
, usurpin beta
, FLICE-like inhibitory protein