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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 (show RTN4 Proteins) 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 (show MLXIP Proteins)-20 and higher CFLAR expression.
Investigations of underlying molecular mechanisms of TNFR1 (show TNFRSF1A Proteins) signaling showed that PDF affects TNFR1 (show TNFRSF1A Proteins) signaling at the proapoptotic signaling pathway by upregulation of IkappaBalpha (show NFKBIA Proteins) 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 (show IRF6 Proteins)+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 (show ROS1 Proteins)-mediated upregulation of DR5 (show TNFRSF10B Proteins) expression, caspase-8 (show CASP8 Proteins) 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 (show PROC Proteins)-FLIPL and regulates the sensitivity of renal cancer cells to various apoptotic stimuli.
Deletion of c-FLIP from CD11b (show ITGAM Proteins)(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 (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.
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