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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

CFLAR CASP8 and FADD-like apoptosis regulator

Top mentioned proteins: FLIP, PrP, caspase-8, CAN, bcl-2
Papers using FLIP antibodies
Distinct signaling pathways in TRAIL- versus tumor necrosis factor-induced apoptosis
Jeremias I et al., In Cell Death & Disease, 2005
... -FLIP (Enzo Life Sciences), α-IκBα (Santa Cruz Technology, Santa Cruz, CA, USA), α-RIP (BD Biosciences), ...
cFLIP regulation of lymphocyte activation and development
Banjerdpongchai Ratana et al., In Journal of Hematology & Oncology, 2005
... Mouse monoclonal antibodies to Mcl-1, BAX and rabbit polyclonal antibody to Bid, cFLIP and horseradish peroxidase (HRP) conjugated secondary antibodies were purchased from Abcam, Cambridge, UK ...
An essential role for c-FLIP in the efficient development of mature T lymphocytes
Eils Roland et al., In Molecular Systems Biology, 2004
... HeLa, HeLa-CD95 and HeLa-CD95–c-FLIPL cells were maintained in DMEM (Life Technologies, Germany), 10 mM HEPES ...
Inhibition of p38 mitogen-activated protein kinase reduces TNF-induced activation of NF-kappaB, elicits caspase activity, and enhances cytotoxicity
Shen Beifen et al., In Molecular Cancer, 2003
... Antibodies against phospho-JNK, JNK, phospho-p38, phospho-CREB, CREB, and c-FLIPL were from Cell Signaling Technology (Beverly, MA, USA) ...
Nuclear Factor of Activated T Cells Balances Angiogenesis Activation and Inhibition
Volpert Olga V. et al., In The Journal of Experimental Medicine, 1997
... Mouse anti–c-FLIP mAb G-11 and goat antiactin pAb I-19 were obtained from Santa Cruz Biotechnology, Inc ...
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Papers on FLIP
Mitochondrial anchorage and fusion contribute to mitochondrial inheritance and quality control in the budding yeast, Saccharomyces cerevisiae.
Pon et al., New York City, United States. In Mol Biol Cell, Feb 2016
Fluorescence loss in photobleaching (FLIP) and network analysis experiments revealed that mitochondria in large buds are a continuous reticulum that is physically distinct from mitochondria in mother cells.
The probiotic Propionibacterium freudenreichii as a new adjuvant for TRAIL-based therapy in colorectal cancer.
Jan et al., Rennes, France. In Oncotarget, Feb 2016
Whole transcriptomic analysis demonstrated that propionibacterial supernatant or propionibacterial metabolites (propionate and acetate), in combination with TRAIL, increased pro-apoptotic gene expression (TRAIL-R2/DR5) and decreased anti-apoptotic gene expression (FLIP, XIAP) in HT29 human colon cancer cells.
Potential of BODIPY-cholesterol for analysis of cholesterol transport and diffusion in living cells.
Stangl et al., Odense, Denmark. In Chem Phys Lipids, Jan 2016
For that purpose, we used a variety of fluorescence approaches including fluorescence correlation spectroscopy and its imaging variants, fluorescence recovery after photobleaching (FRAP) and fluorescence loss in photobleaching (FLIP).
Simultaneous gene silencing of KRAS and anti-apoptotic genes as a multitarget therapy.
Pilarsky et al., Dresden, Germany. In Oncotarget, Jan 2016
Therefore multimodal therapy strategies, targeting signaling pathways simultaneously should improve treatment.SiRNAs against KRAS and the apoptosis associated genes BCLXL, FLIP, MCL1L, SURVIVIN and XIAP were transfected into human and murine pancreatic cancer cell lines.
Dual modulation of Ras-Mnk and PI3K-AKT-mTOR pathways: A Novel c-FLIP inhibitory mechanism of 3-AWA mediated translational attenuation through dephosphorylation of eIF4E.
Goswami et al., New Delhi, India. In Sci Rep, Dec 2015
Herein, we demonstrate that medicinal plant derivative 3-AWA (from Withaferin A) suppressed the proliferation and metastasis of CaP cells through abrogation of eIF4E activation and expression via c-FLIP dependent mechanism.
Functional conservation of the apoptotic machinery from coral to man: the diverse and complex Bcl-2 and caspase repertoires of Acropora millepora.
Miller et al., Townsville, Australia. In Bmc Genomics, Dec 2015
Structure prediction suggests that the active and inactive caspase domains in caspase-X are likely to interact, resulting in a structure resembling that of the active domain in procaspase-8 and the inactive caspase domain in the mammalian c-FLIP anti-apoptotic factor.
Biology and oncogenicity of the Kaposi sarcoma herpesvirus K1 protein.
Elgui De Oliveira et al., Botucatu, Brazil. In Rev Med Virol, Sep 2015
KSHV is unique among other human herpesviruses because of the elevated number of viral products that mimic human cellular proteins, such as a viral cyclin, a viral G protein-coupled receptor, anti-apoptotic proteins (e.g., v-bcl2 and v-FLIP), viral interferon regulatory factors, and CC chemokine viral homologues.
Myeloid-derived suppressor activity is mediated by monocytic lineages maintained by continuous inhibition of extrinsic and intrinsic death pathways.
Murray et al., Memphis, United States. In Immunity, 2015
Using genetic manipulation of cell death pathways, we found the monocytic suppressor-cell subset, but not the granulocytic subset, requires continuous c-FLIP expression to prevent caspase-8-dependent, RIPK3-independent cell death.
Lesser-Known Molecules in Ovarian Carcinogenesis.
Căruntu et al., Jászvásár, Romania. In Biomed Res Int, 2014
Within this framework, this review presents three protein molecules: ALCAM, c-FLIP, and caveolin, motivated by the perspectives provided through the current limited knowledge on their role in ovarian carcinogenesis and on their potential as prognosis factors.
DED or alive: assembly and regulation of the death effector domain complexes.
Longley et al., Belfast, United Kingdom. In Cell Death Dis, 2014
Death effector domains (DEDs) are protein-protein interaction domains initially identified in proteins such as FADD, FLIP and caspase-8 involved in regulating apoptosis.
FLIP the Switch: Regulation of Apoptosis and Necroptosis by cFLIP.
Nakano et al., Tokyo, Japan. In Int J Mol Sci, 2014
cFLIP (cellular FLICE-like inhibitory protein) is structurally related to caspase-8 but lacks proteolytic activity due to multiple amino acid substitutions of catalytically important residues.
A long-awaited merger of the pathways mediating host defence and programmed cell death.
Blander, New York City, United States. In Nat Rev Immunol, 2014
Molecules such as receptor-interacting protein kinase 1 (RIPK1), RIPK3, FAS-associated death domain protein (FADD), FLICE-like inhibitory protein (FLIP) and caspase 8 - which are associated with different forms of cell death - are incorporated into compatible and exceedingly dynamic Toll-like receptor, NOD-like receptor and RIG-I-like receptor signalling modules.
Tumor endothelium FasL establishes a selective immune barrier promoting tolerance in tumors.
Coukos et al., Philadelphia, United States. In Nat Med, 2014
Tumor-derived vascular endothelial growth factor A (VEGF-A), interleukin 10 (IL-10) and prostaglandin E2 (PGE2) cooperatively induced FasL expression in endothelial cells, which acquired the ability to kill effector CD8(+) T cells but not Treg cells because of higher levels of c-FLIP expression in Treg cells.
Systematic identification of molecular subtype-selective vulnerabilities in non-small-cell lung cancer.
White et al., Dallas, United States. In Cell, 2013
These include NLRP3 mutation/inflammasome activation-dependent FLIP addiction, co-occurring KRAS and LKB1 mutation-driven COPI addiction, and selective sensitivity to a synthetic indolotriazine that is specified by a seven-gene expression signature.
Direct measurement of DNA affinity landscapes on a high-throughput sequencing instrument.
Burge et al., Cambridge, United States. In Nat Biotechnol, 2011
Here we describe 'high-throughput sequencing'-'fluorescent ligand interaction profiling' (HiTS-FLIP), a technique for measuring quantitative protein-DNA binding affinity at unprecedented depth.
Expression and localization of cFLIP, an anti-apoptotic factor, in the bovine corpus luteum.
Okuda et al., Okayama, Japan. In J Reprod Dev, 2010
results indicate downregulation of cFLIP during structural luteal regression, suggesting that cFLIP plays a survival role in the bovine corpus luteum
Sequencing, chromosomal mapping, and functional characterization of bovine FLICE-like inhibitory protein (FLIP).
Bannerman et al., Beltsville, United States. In Cytogenet Genome Res, 2005
Conservation of FLIP's ability to inhibit apoptosis and to downregulate NF-kappaB activation across species.
More papers using FLIP antibodies
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