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cFLIP appears to bind to IKKalpha to prevent IKKalpha from phosphorylating and activating IRF7.
High c-FLIP expression is associated with resistance to sorafenib via reducing ER stressrelated autophagy in hepatocellular carcinoma.
TRAIL synergistically sensitized irradiation-induced apoptosis in glioblastoma stem-like cells by increasing DR5 expression and decreasing cFLIP expression.
The knockdown of endogenous c-FLIP revealed that this protein regulates hepatitis B virus replication through two different mechanisms. (i) c-FLIP interacts with HBx and protects it from ubiquitin-dependent degradation. (ii) c-FLIP regulates the expression or stability of hepatocyte nuclear factors (HNFs), which have critical roles in HBV transcription and maintenance of hepatocytes.
Nogo-B was shown to play an important negative role in apoptotic signaling through its interaction with c-FLIP in colorectal cancer cells.
Compared to normal tissues, hepatocellular carcinoma tissues had lower miR-20 and higher CFLAR expression.
Investigations of underlying molecular mechanisms of TNFR1 signaling showed that PDF affects TNFR1 signaling at the proapoptotic signaling pathway by upregulation of IkappaBalpha and downregulation of cFLIPL.
c-FLIP expression was significantly decreased in organs of septic rats compared with control rats, and that c-FLIP overexpression protected HUVECs from LPS+CHX-induced apoptosis in vitro.
case-control study, including 600 hepatocellular carcinoma (HCC) and 600 HBsAg positive controls without HCC, was conducted to assess the relationship between 11 tagging SNPs in CASP8, CASP10 and CFLAR and HBV-related HCC risk .These results suggest that the CASP8 -652 6N ins/del polymorphism may play a protective role in the development, progression, and survival of HBV-related HCC among the Chinese Han population.
we found that plumbagin could enhance TRAIL-induced apoptosis in Kasumi-1 cells, and the mechanisms include ROS-mediated upregulation of DR5 expression, caspase-8 activation and inhibition of cFLIP expression
Cordycepin induces apoptosis through autophagy-mediated downregulation of c-FLIPL in human non-small cell lung carcinoma cells.
High c-FLIP expression is associated with lung cancer.
miRNA-708 acts as a tumor suppressor because it negatively regulates the anti-apoptotic protein c-FLIPL and regulates the sensitivity of renal cancer cells to various apoptotic stimuli.
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/Mcl-1 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 with Beclin-1 and substantiates p53 dependent ubiquitination of Beclin-1 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 and caspase-8 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), a transcription factor central for IFN-beta and IFN-stimulated gene expression.
Deletion of c-FLIP from CD11b(hi) Macrophages Prevents Development of Bleomycin-induced Lung Fibrosis.
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 dimerization are new and feasible approaches for NASH treatment.
knockdown of cFLIPL and induced expression of FADD rapidly accumulate intracellular ROS accompanied by JNK1 activation to substantiate apoptosis.
CASP8 is present exclusively as its cleaved p43 product, bound to cFLIPL.
The generation of mouse line with Flip deficiency in cells that express cre under the CD11c promoter is reported.
c-FLIPL deficiency induces the caspase-mediated processing of RTN4, 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.
Upon starvation, c-Flip affects lipid accumulation, ER stress and autophagy, thereby pointing to an important role of c-Flip in the adaptive response and ER stress response programs under both normal and pathological conditions.
Flip preserves cardiac functions and inhibits cardiac hypertrophy partially by blocking ASK1/P38 signaling.
These data suggest that c-FLIP is a negative regulator of intrinsic apoptosis pathway in T lymphocytes.
c-FLIPR is an important modulator of apoptosis and enforced expression leads to autoimmunity.
controls the development of monocyte-derived myeloid suppressor cells; constitutive expression distinguishes tumor-resident cells
cFLIP protein expression from one allele of cFLIP is sufficient to protect epidermal keratinocytes from cell death and a macroscopic phenotype upon acute ablation of the cFLIP locus.
Data indicate that caspase-8 activity is lost upon deletion of c-FLIPL, and p43FLIP rescues caspase-8 activity through Raf1, TRAF2, and RIPK1 association, augmenting ERK and NF-kappaB pathways.
cFLIP regulates cellular injury from apoptosis signaling pathways.
Cellular FLICE-like inhibitory protein secures intestinal epithelial cell survival and immune homeostasis by regulating caspase-8.
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 activation across species.
We propose that cFLIPS/L acts as a survival factor, and performs an anti-apoptotic function in the porcine corpora lutea.
cFLIPs play important roles in the regulation mechanism of apoptosis in ovarian follicular granulosa cells.
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-FLIP in xenograft cells may decrease the innate cellular responses against xenografts, facilitating long-term xenograft survival.
pcFLIP acts as a survival-promoting factor in granulosa cells and determines whether porcine ovarian follicles survive or undergo atresia.
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.
Overexpression of the antiapoptotic molecules, pig FLIPs, has the potential for use in protecting graft cells from human natural killer cells in xenografts.
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