Ignet

Gene Information

Gene symbol: CFLAR

Gene name: CASP8 and FADD-like apoptosis regulator

HGNC ID: 1876

Synonyms: CASH, Casper, CLARP, FLAME, FLIP, I-FLICE, MRIT, c-FLIP

Related Genes

#	Gene Symbol	Number of hits
1	BCL2	1 hits
2	BCL2A1	1 hits
3	CASP2	1 hits
4	CASP8	1 hits
5	CAST	1 hits
6	CCL4	1 hits
7	CDK2	1 hits
8	EIF3E	1 hits
9	FADD	1 hits
10	FASLG	1 hits
11	GADD45B	1 hits
12	HMGB1	1 hits
13	IL1B	1 hits
14	NFKB1	1 hits
15	NFKB2	1 hits
16	PIM2	1 hits
17	RAF1	1 hits
18	RELA	1 hits
19	SOD2	1 hits
20	TNFAIP3	1 hits
21	TNFRSF10C	1 hits
22	TNFRSF10D	1 hits
23	TNFSF10	1 hits
24	VEGFA	1 hits
25	XIAP	1 hits

Related Sentences

#	PMID	Sentence
1	16081851	Mice bearing intracranial GL261 glioma or MCA205 sarcoma received peripheral immunizations with corresponding irradiated tumor cells engineered to express IL-4 or GM-CSFs, respectively, as well as intratumoral delivery of DC-IFN-alpha.
2	16081851	This regimen prolonged survival of the animals and induced tumor-specific CTLs that expressed TRAIL, which in concert with perforin and Fas ligand (FasL) was involved in the tumor-specific CTL activity of these cells.
3	16081851	The in vivo antitumor activity associated with this approach was abrogated by administration of neutralizing mAbs against TRAIL or FasL and was not observed in perforin-/-, IFN-gamma-/-, or FasL-/- mice.
4	16081851	Transduction of the tumor cells with antiapoptotic protein cellular FLIP rendered the gene-modified cells resistant to TRAIL- or FasL-mediated apoptosis and to CTL killing activity in vitro.
5	20119528	FLIP (FLICE-inhibitory protein), anti-apoptotic members of the Bcl2 family and inhibitors of apoptosis (IAP) are the main three groups of anti-apoptotic genes that counteract caspase activation through both the extrinsic and intrinsic apoptotic pathways.Modulation of the apoptotic machinery during viral and bacterial infections, as well as in various malignancies, is a wellestablished mechanism that promotes the survival of affected cells.
6	20419158	Escape of HIV-1-infected dendritic cells from TRAIL-mediated NK cell cytotoxicity during NK-DC cross-talk--a pivotal role of HMGB1.
7	20419158	We first addressed the question of the mechanisms involved in iDC editing, and we show that cognate NK-iDC interaction triggers apoptosis via the TNF-related apoptosis-inducing ligand (TRAIL)-Death Receptor 4 (DR4) pathway and not via the perforin pathway.
8	20419158	This resistance occurs despite normal amounts of TRAIL released by NK cells and comparable DR4 expression on DC(HIV).
9	20419158	High-mobility group box 1 (HMGB1), an alarmin and a key mediator of NK-DC cross-talk, was found to play a pivotal role in NK-dependent upregulation of c-FLIP and c-IAP2 in DC(HIV).
10	20419158	Finally, we demonstrate that restoration of DC(HIV) susceptibility to NK-induced TRAIL killing can be obtained either by silencing c-FLIP and c-IAP2 by specific siRNA, or by inhibiting HMGB1 with blocking antibodies or glycyrrhizin, arguing for a key role of HMGB1 in TRAIL resistance and DC(HIV) survival.
11	20419158	Escape of HIV-1-infected dendritic cells from TRAIL-mediated NK cell cytotoxicity during NK-DC cross-talk--a pivotal role of HMGB1.
12	20419158	We first addressed the question of the mechanisms involved in iDC editing, and we show that cognate NK-iDC interaction triggers apoptosis via the TNF-related apoptosis-inducing ligand (TRAIL)-Death Receptor 4 (DR4) pathway and not via the perforin pathway.
13	20419158	This resistance occurs despite normal amounts of TRAIL released by NK cells and comparable DR4 expression on DC(HIV).
14	20419158	High-mobility group box 1 (HMGB1), an alarmin and a key mediator of NK-DC cross-talk, was found to play a pivotal role in NK-dependent upregulation of c-FLIP and c-IAP2 in DC(HIV).
15	20419158	Finally, we demonstrate that restoration of DC(HIV) susceptibility to NK-induced TRAIL killing can be obtained either by silencing c-FLIP and c-IAP2 by specific siRNA, or by inhibiting HMGB1 with blocking antibodies or glycyrrhizin, arguing for a key role of HMGB1 in TRAIL resistance and DC(HIV) survival.
16	21881300	Moreover, PLGA microcapsules of siRNAs against VEGF, cFLIP, Raf-1, and Int6 have also been developed to treat various cancers and arteriosclerosis obliterans.
17	21881300	To develop therapeutic nucleotides, a particle design is created using functional peptides, such as cell penetrating peptides (CPP), nuclear localizing signals (NLS), tight junction reversible openers (AT1002), bombesin, and dynein light chain-associated sequences. siRNA use should lead to a paradigm shift in drug discovery against various diseases.
18	22986450	Specific targets in this category included genes asso-ciated with the intrinsic and extrinsic apoptotic pathways (CFLAR, TNFAIP3, TNFRSF10D, SOD2, BCL2A1, BIRC4, PIM2, TNFSF10, TNFRSF10C, CASP2 and CASP8) and genes that act via the NFĸB pathway and other mechanisms to prolong cell viability (NFKB1, NFKB2 and RELA, IL1B, CAST, CDK2,GADD45B, BCL3, BIRC3, CDK2, IL1A, PBEF1, IL6, CXCL1, CCL4 and VEGF).
19	22986450	Moreover, we demonstrate that the X-linked inhibitor of apoptosis protein remained abundant in polymorphonuclear leukocytes over 48 h of LVS infection, whereas BAX mRNA and protein were progressively downregulated.
20	25807052	Whereas Fas or FasL knockout mice had improved CMI, down-regulation of Fas or FasL by shRNA or antibody failed to improve CMI and was accompanied by increases in regulatory T cells (Treg).
21	25807052	The adjuvant effects of Fas-associated death domain (FADD) and of cellular FLICE-inhibitory protein (cFLIP) were consistently accompanied by increased effector memory T lymphocytes and increased T cell proliferation.
22	25807052	However, half of the mice pre-electroporated with FADD or cFLIP plasmids were able to clear LCMV-Clone 13 by day nine, and, in the case of cFLIP, increased viral clearance was accompanied by higher CMI.
23	25807052	Whereas Fas or FasL knockout mice had improved CMI, down-regulation of Fas or FasL by shRNA or antibody failed to improve CMI and was accompanied by increases in regulatory T cells (Treg).
24	25807052	The adjuvant effects of Fas-associated death domain (FADD) and of cellular FLICE-inhibitory protein (cFLIP) were consistently accompanied by increased effector memory T lymphocytes and increased T cell proliferation.
25	25807052	However, half of the mice pre-electroporated with FADD or cFLIP plasmids were able to clear LCMV-Clone 13 by day nine, and, in the case of cFLIP, increased viral clearance was accompanied by higher CMI.