ライフサイエンスコーパス: FLIP

1 FLIP is a well-established suppressor of death receptor-

2 FLIP silencing-induced caspase 8 activation in Bax wild-

3 FLIP studies also showed that mitochondria that enter th

4 FLIP(S) half-life in PTEN mutant GBM cells was reduced b

5 FLIPs are a family of viral and cellular proteins initia

6 regulation is postulated, but exactly how a FLIP performs such multifunctional roles remains to be e

7 Moreover, silencing of Cbl abrogated FLIP(S) reduction induced by rictor knockdown.

8 , an event previously shown to increase AIP4-FLIP(S) interaction, whereas siRNA-mediated suppression

9 vate antiapoptotic genes, including BCL2 and FLIP.

10 Caspase-8, FADD, and FLIP orchestrate apoptosis in response to death receptor

11 the mechanism by which caspase-8, FADD, and FLIP prevent runaway RIPK activation is unknown, and the

12 the lethal defect in caspase-8-, FADD-, and FLIP-deficient animals and tissues.

13 In macrophages, FLIP long (FLIP(L)) and FLIP short (FLIP(S)) mRNA was induced by tumor necrosis

14 termine whether the use of the SAF score and FLIP algorithm can decrease interobserver variations amo

15 n Group 2 after the use of the SAF score and FLIP algorithm.

16 Survivin and FLIP anti-apoptotic factors, vascular endothelial growth

17 c-FLIP silencing with anti-FLIP short interfering RNA (siRNA) in pulmonary MVECs re

18 TRAIL, and antiapoptotic molecules, such as FLIP and Bcl-xL, in inflammatory cells from thyroids of

19 ells, were not sensitized to these agents by FLIP silencing.

20 It is negatively regulated by FLIP, cIAP1, cIAP2, and XIAP.

21 c-FLIP can inhibit death receptor-mediated apoptosis by co

22 c-FLIP may inhibit or promote T cell death as previous dat

23 c-FLIP protein levels are regulated by ubiquitination and

24 c-FLIP silencing with anti-FLIP short interfering RNA (siR

25 c-FLIP(f/f) LysM-Cre mice exhibit delayed clearance of cir

26 c-FLIP(L)(-/-) mice exhibit severely impaired effector T c

27 Although c-FLIP has been identified as an important player in the e

28 e1 expressed increased levels of Bcl-2 and c-FLIP and decreased levels of Fas RNA compared with HKIR

29 positive cross-talk exists between Akt and c-FLIP in the context of inhibition of FasL-induced NF-kap

30 steria monocytogenes infection in vivo and c-FLIP(L)-deficient T cells display defective TCR-mediated

31 ted antiapoptotic genes bfl-1, cIAP-2, and c-FLIP.

32 re differentially regulated by cIAP1/2 and c-FLIP.

33 ase inhibitors was sufficient to attenuate c-FLIP levels.

34 and that gamma-secretase inhibitor blocked c-FLIP turnover and also partially blocked PS1-induced apo

35 assembly and activation are controlled by c-FLIP isoforms, which function as pro-apoptotic (c-FLIPL

36 /TRAIL can be restored at least in part by c-FLIP pathway inhibitors.

37 The active caspase.c-FLIP complex forms in the absence of Fas (CD95/APO1) and

38 e granulocytic subset, requires continuous c-FLIP expression to prevent caspase-8-dependent, RIPK3-in

39 We found that celecoxib controlled c-FLIP ubiquitination through Akt-independent inhibition o

40 itiator caspase activation and cell death, c-FLIP(L) is also capable of enhancing procaspase-8 activa

41 s of other related proteins including DR4, c-FLIP, FADD, and caspase-8.

42 onstrate that acute deletion of endogenous c-FLIP in murine effector T cells results in loss of caspa

43 -8 activation is not blocked by endogenous c-FLIP.

44 een NF-kappaB and PI3K/Akt and establishes c-FLIP as an important regulator of FasL-mediated cell dea

45 ing CD95 expression or in cells expressing c-FLIP-s, the lethality of sorafenib + HDACI exposure was

46 d by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1.

47 lthough the long isoform of cellular FLIP (c-FLIP(L)) has been implicated in TCR-mediated signaling,

48 ing enzyme inhibitory protein, short form (c-FLIP-s) blocked enhanced killing.

49 sion of endogenous NF-kappaB target genes (c-FLIP, TRAF1), and resistance to apoptosis.

50 role of c-FLIPL and crucially defines how c-FLIP isoforms differentially control cell fate.

51 However, c-FLIP(L)(-/-) T cells exhibit normal NF-kappaB activity u

52 xygen species (ROS) has been implicated in c-FLIP protein degradation.

53 or increase in reactive oxygen species in c-FLIP-deficient resting T cells.

54 deletion rescued the enhanced apoptosis in c-FLIP-deficient T cells, whereas inhibition of caspase 8

55 ed apoptosis in association with increased c-FLIP levels.

56 e effects of GSK3 inhibition and increased c-FLIP ubiquitination, confirming that c-FLIP attenuation

57 pletion of TRAF7 correlates with increased c-FLIP(L) expression level, which, in turn, results in res

58 ated with the intrinsic apoptosis inducer, c-FLIP suppressed cytochrome c release from mitochondria.

59 repression of cellular caspase-8 inhibitor c-FLIP (also known as CFLAR) expression through activation

60 liminating endogenous caspase-8 inhibitor, c-FLIP, while Smac mimetic does so by triggering autodegra

61 Thus, not only is c-FLIP the initiator of caspase-8 activity during T cell a

62 knockout mouse strain specifically lacking c-FLIP(L) in T lymphocytes.

63 ne sulfoximine down-regulates c-FLIP long (c-FLIP(L)) protein levels, which is prevented by the prote

64 n were found to be important for mediating c-FLIP-dependent downregulation of NF-kappaB activity.

65 rthermore, the expression of Mcl-1 but not c-FLIP was significantly reduced when COX-2 was suppressed

66 reduced the abundance of the short form of c-FLIP (FLIP(S), CFLAR(S)) and survivin (BIRC5).

67 th GSK3 inhibition enhanced attenuation of c-FLIP and increased apoptosis.

68 atment resulted in decreased expression of c-FLIP and Mcl-1, which were determined to be transcriptio

69 presence of two death effector domains of c-FLIP and S-nitrosylation of its caspase-like domain were

70 -dependent pathway mediated by turnover of c-FLIP and the gamma-secretase-independent pathway mediate

71 this protein in regulating the turnover of c-FLIP and, consequently, cell death.

72 mediated apoptosis, while up-regulation of c-FLIP by gene transfer partially protected dermal MVECs f

73 Inhibition of c-FLIP by means of RNA interference increased Apo2/TRAIL s

74 o involve cytokine-induced acceleration of c-FLIP degradation, sensitizing cells to TRAIL-mediated ca

75 not Treg cells because of higher levels of c-FLIP expression in Treg cells.

76 To investigate the function of c-FLIP in mature T cells, we have generated several geneti

77 sm through which the regulatory effects of c-FLIP on death receptor signaling are controlled by GSK3,

78 ion of NF-kappaB through overexpression of c-FLIP or IKK (also known as CFLAR and IKBKB, respectively

79 Short hairpin RNA-mediated knockdown of c-FLIP or Mcl-1 significantly sensitized these cells to TR

80 re T lymphocytes in vitro, and the role of c-FLIP protein in intrinsic apoptosis pathway was studied.

81 Accordingly, expression of c-FLIP T166A or K167R mutants protected cells from ROS-med

82 Moreover, down-regulation of c-FLIP using small interfering RNA in nonactivated T cells

83 structures of the protease-like domain of c-FLIP(L) alone and in complex with zymogen C8 identify th

84 LIP(L) and demonstrate that degradation of c-FLIP(L) also occurs through a lysosomal pathway.

85 hat cleavage of the intersubunit linker of c-FLIP(L) by procaspase-8 potentiates the activation proce

86 de molecular insights into a key aspect of c-FLIP(L) function that modulates procaspase-8 activation

87 sine 167 as a novel ubiquitination site of c-FLIP(L) important for ROS-dependent degradation.

88 To establish the role of c-FLIP(L) in T lymphocyte proliferation, we have generated

89 s have demonstrated that overexpression of c-FLIP(L) promotes T cell proliferation and NF-kappaB acti

90 enger prevented ubiquitination and loss of c-FLIP(L) protein induced by menadione or paraquat.

91 ATL by transcriptional down-regulation of c-FLIP, a key inhibitor of death receptor signaling, and b

92 with ABT-737 did not change the levels of c-FLIP, FADD, and caspase-8 but up-regulated the levels of

93 ity in association with down-regulation of c-FLIP, suggesting that c-FLIP synthesis, not intracellula

94 Overexpression of c-FLIP-s or loss of BID function suppressed BBR3610 toxici

95 this may be mediated by down-regulation of c-FLIP.

96 ectin, soluble factor(s) have no impact on c-FLIP redistribution within cellular compartments.

97 s and selective knockdown of either RIP or c-FLIP with interfering RNA redistributes the DISC from no

98 substrate repertoire, limited to itself or c-FLIP.

99 The caspase-8 paralogue c-FLIP is a good candidate for a molecular rheostat of cas

100 that fail to activate caspase-8 and permit c-FLIP(L) cleavage cannot facilitate NF-kappaB activation

101 The cytosolic protein c-FLIP (cellular Fas-associated death domain-like interleu

102 eline levels of the anti-apoptotic protein c-FLIP in all cell lines tested.

103 Cellular FLICE-inhibitory protein (c-FLIP(L)) is a key regulator of the extrinsic cell death

104 of cellular FLICE-like inhibitory protein (c-FLIP) and Mcl-1.

105 optosis regulator-like inhibitory protein (c-FLIP) and myeloid cell leukemia 1 (Mcl-1).

106 ne cellular FLICE-like inhibitory protein (C-FLIP) in myeloid cells, we have generated a novel mouse

107 caspase 8 (FLICE)-like inhibitory protein (c-FLIP) is required for TNFalpha-induced protection agains

108 beta-converting enzyme-inhibitory protein (c-FLIP) mediates the DISC assembly in nonrafts and selecti

109 caspase 8 (FLICE)-like inhibitory protein (c-FLIP) promotes cell survival in death receptor-induced a

110 th cellular FLICE-like inhibitory protein (c-FLIP) turnover and that gamma-secretase inhibitor blocke

111 tion of cellular FLICE-inhibitory protein (c-FLIP), a major regulator of the death receptor pathway o

112 Cellular FLICE-inhibitory protein (c-FLIP), an antioxidant and an important component of the

113 tion of cellular FLICE inhibitory protein (c-FLIP), an inhibitor of apoptosis.

114 or cellular FLICE-like inhibitory protein (c-FLIP), targeting it for proteasome degradation.

115 ease in cellular FLICE-inhibitory protein (c-FLIP).

116 of cellular FLICE-like inhibitory protein (c-FLIP-s) or knockdown of CD95 suppressed the lethality of

117 of cellular FLICE-like inhibitory protein (c-FLIP-s).

118 iquitination of the anti-apoptotic protein c-FLIP(L) and demonstrate that degradation of c-FLIP(L) al

119 pases-8 and -10 and the regulatory protein c-FLIP.

120 APL cells, in which PMLRARalpha recruited c-FLIP(L/S) and excluded procaspase 8 from Fas death signa

121 use TGM2 suppression significantly reduced c-FLIP but not Mcl-1 expression.

122 ent caused DISC formation without reducing c-FLIP-s expression and did not increase CD95 plasma membr

123 which ROS post-transcriptionally regulate c-FLIP protein levels is not well understood.

124 ssential for soluble factor(s) to regulate c-FLIP.

125 , or buthionine sulfoximine down-regulates c-FLIP long (c-FLIP(L)) protein levels, which is prevented

126 166 or Lys-167 was sufficient to stabilize c-FLIP protein levels in PPC-1, HEK293T, and HeLa cancer c

127 In this study, c-FLIP gene was deleted in mature T lymphocytes in vitro,

128 ng therapeutic potential, act by targeting c-FLIP ubiquitination and degradation by the proteasome.

129 sed c-FLIP ubiquitination, confirming that c-FLIP attenuation was mediated by proteasomal turnover as

130 Current models assume that c-FLIP directly competes with procaspase-8 for recruitment

131 Our results demonstrate that c-FLIP functions beyond the extrinsic death pathway.

132 These data suggest that c-FLIP is a negative regulator of intrinsic apoptosis path

133 Surprisingly, we found that c-FLIP protects mature T cells not only from apoptosis ind

134 down-regulation of c-FLIP, suggesting that c-FLIP synthesis, not intracellular traffic, is essential

135 These results demonstrate that c-FLIP(L) is essential for T lymphocyte proliferation thro

136 ivation, whereas others have reported that c-FLIP(L) overexpression has no effect or even inhibits T

137 nt post-translational modifications of the c-FLIP protein that regulate its stability, thus impacting

138 eath as previous data demonstrate that the c-FLIP(L) isoform can promote or inhibit caspase 8 activat

139 Although the c-FLIP(R) isoform inhibits cell death in cell lines, its f

140 or inhibit caspase 8 activation while the c-FLIP(S) isoform promotes or inhibits T cell death when o

141 ediated TRAIL resistance is likely through c-FLIP because TGM2 suppression significantly reduced c-FL

142 Thus, c-FLIP plays an essential role in protecting mature T cell

143 not alter the activity of caspase-8 toward c-FLIP(L), which is required for antigenic signaling.

144 Whether c-FLIP regulates mitochondrion-dependent apoptotic signals

145 enerated several genetic mouse models with c-FLIP or its individual isoforms deleted in mature T cell

146 rming an apoptotic inhibitory complex with c-FLIP.

147 Total levels of the candidate FLIP(S) E3 ubiquitin ligase atrophin-interacting protein

148 However, CD2-FLIP Tg(+) donors often transferred less severe G-EAT, e

149 Cellular FLIP (cFLIP) forms are also known to activate the NF-kap

150 Cellular FLIP (cFLIP) is a homolog of caspase 8 and is also capab

151 Cellular FLIP (Flice-like inhibitory protein) is critical for the

152 els of the Fas-signaling antagonist cellular FLIP (cFLIP) in germinal center (GC) B cells suggests an

153 2), cell survival (Bcl-2, Bcl-x(L), cellular FLIP, inhibitor of apoptosis protein 1, inhibitor of apo

154 Although the long isoform of cellular FLIP (c-FLIP(L)) has been implicated in TCR-mediated sig

155 The cellular FLIP long isoform protein (cFLIPL) controls type I IFN p

156 ng TRAIL exposure, HSP90alpha and the client FLIP(S) protein were recruited to the death-inducing sig

157 kt, regulates the ability of AIP4 to control FLIP(S) stability and TRAIL sensitivity.

158 IP(S) ubiquitination, USP8 seemed to control FLIP(S) ubiquitination through an intermediate target.

159 Here, we present CRISPR-FLIP, a strategy that provides an efficient, rapid and s

160 on of AIP4 levels in PTEN WT cells decreased FLIP(S) ubiquitination, prolonged FLIP(S) half-life, and

161 Rictor knockdown decreased FLIP(S) stability, whereas enforced expression of rictor

162 tion, decreased FLIP(S) half-life, decreased FLIP(S) steady-state levels, and decreased TRAIL resista

163 PP242 decreased FLIP(S) stability, increased FLIP(S) ubiquitination, and

164 increased FLIP(S) ubiquitination, decreased FLIP(S) half-life, decreased FLIP(S) steady-state levels

165 s longer half-life correlated with decreased FLIP(S) polyubiquitination.

166 but not raptor, mimicked PP242 in decreasing FLIP(S) levels and sensitizing cells to TRAIL.

167 3 mutation/inflammasome activation-dependent FLIP addiction, co-occurring KRAS and LKB1 mutation-driv

168 ble form of FOXO3a (FOXO3aTM), downregulates FLIP protein and mRNA.

169 Enforced expression of ectopic FLIP(S), but not survivin, attenuated augmented apoptosi

170 etylase 1 (HDAC1) or HDAC3 on the endogenous FLIP promoter but not in mice lacking p50.

171 uitment, the FADD DED preferentially engages FLIP using its alpha1/alpha4 surface and procaspase 8 us

172 Moreover, TNFalpha enhanced FLIP(L) serine phosphorylation, which was increased by a

173 Here we examine FLIPs (MC159 and MC160) encoded by the molluscum contagi

174 (59 of 60) of human STS specimens exhibited FLIP expression, suggesting that the nuclear IRF8 protei

175 ased FLIP(S) ubiquitination, and facilitated FLIP(S) degradation.

176 The DEDs of FADD, FLIP and procaspase 8 interact with one another using tw

177 d the abundance of the short form of c-FLIP (FLIP(S), CFLAR(S)) and survivin (BIRC5).

178 caspase 3 processing and apoptosis following FLIP silencing.

179 We show herein that ROS are required for FLIP down-regulation and apoptosis induction by Fas liga

180 a primary oxidative species responsible for FLIP down-regulation, whereas superoxide serves as a sou

181 activity, identifying a unique function for FLIPs.

182 As such, a broad role for FLIPs in disease regulation is postulated, but exactly h

183 ata were exported to software that generated FLIP topography plots.

184 pressed and CDDP failed to abolish the I-GSN-FLIP-Itch interaction, resulting in the dysregulation of

185 sistance in cancer cells by altering the GSN-FLIP-Itch interaction.

186 Application of HiTS-FLIP to the protein Gcn4 (Gcn4p), the master regulator o

187 orescent ligand interaction profiling' (HiTS-FLIP), a technique for measuring quantitative protein-DN

188 We hypothesized that if FLIP were overexpressed on lymphocytes, CD4(+) effector

189 ent disease, G-EAT resolution was delayed in FLIP transgenic mice.

190 that it is mTORC2 inhibition that results in FLIP(S) downregulation and subsequent sensitization of T

191 73, a putative Akt-1 phosphorylation site in FLIP(L), was critical for the activation-induced reducti

192 from IRF8-null mice also exhibited increased FLIP protein level, suggesting that IRF8 might be a gene

193 PP242 decreased FLIP(S) stability, increased FLIP(S) ubiquitination, and facilitated FLIP(S) degradat

194 g expression of FOXO3aTM, leads to increased FLIP expression.

195 but increased AIP4 ubiquitination, increased FLIP(S) steady-state levels, and suppressed FLIP(S) ubiq

196 t not catalytically inactive USP8, increased FLIP(S) ubiquitination, decreased FLIP(S) half-life, dec

197 rupting IRF8 function dramatically increases FLIP mRNA stability, resulting in increased IRF8 protein

198 E3 ligase Cbl (CBL) abolished PP242-induced FLIP(S) reduction.

199 by CDDP in sensitive cells, thereby inducing FLIP ubiquitination and degradation, followed by apoptos

200 d superoxide dismutase effectively inhibited FLIP down-regulation and apoptosis induction by FasL.

201 s the DEDs of procaspase 8 and its inhibitor FLIP to form death-inducing signalling complexes (DISCs)

202 Thus, it is FLIP(S) downregulation that contributes to synergistic i

203 results show that HSP90alpha, by localizing FLIP(S) to the DISC, plays a key role in the resistance

204 In macrophages, FLIP long (FLIP(L)) and FLIP short (FLIP(S)) mRNA was induced by tu

205 lex with FLICE-like inhibitory protein long (FLIP(L), also known as CFLAR), and this complex is requi

206 In macrophages, FLIP long (FLIP(L)) and FLIP short (FLIP(S)) mRNA was in

207 ogether, our data suggest that IRF8 mediates FLIP expression level to regulate apoptosis and targetin

208 educed the protein level of FLIP(L), but not FLIP(S), at 1 and 2 h.

209 ith Tg(-) littermates, presumably because of FLIP overexpression on B cells.

210 complex and the degradation and cleavage of FLIP, an inhibitor of caspase-8, in renal cystic epithel

211 -disk confocal imaging with a combination of FLIP, FRAP, and photoactivatable GFP-Bax, we demonstrate

212 , PP242 induces Cbl-dependent degradation of FLIP(S), leading to FLIP(S) downregulation.

213 studies indicated the site of expression of FLIP and Fas ligand [thyroid epithelial cells (TECs) ver

214 served TNFalpha reduced the protein level of FLIP(L), but not FLIP(S), at 1 and 2 h.

215 eubiquitinase correlated with high levels of FLIP(S) ubiquitination, USP8 seemed to control FLIP(S) u

216 Transgenic overexpression of FLIP protected cultured splenocytes from Fas-mediated, b

217 poptosis due to transgenic overexpression of FLIP.

218 her, our results indicate a novel pathway of FLIP regulation by an interactive network of reactive ox

219 t TNF was protective only in the presence of FLIP(L).

220 The reduction of FLIP(L) by TNFalpha was not mediated by caspase 8, or th

221 ere by TNFalpha facilitates the reduction of FLIP(L) protein, which is dependent on the phosphatidyli

222 The reduction of FLIP(L) resulted in the short term induction of caspase

223 ical for the activation-induced reduction of FLIP(L).

224 ROS mediate the down-regulation of FLIP by ubiquitination and subsequent degradation by pro

225 USP8 links Akt to AIP4 and the regulation of FLIP(S) stability and TRAIL resistance.

226 PTEN-Akt-AIP4 pathway as a key regulator of FLIP(S) ubiquitination, FLIP(S) stability, and TRAIL sen

227 ng that IRF8 might be a general repressor of FLIP.

228 Deletion of JNK led to the stabilization of FLIP L, reduced caspase-8 activation, decreased Bid clea

229 Furthermore, the suppression of FLIP(S) levels by USP8 overexpression was reversed by th

230 en interact via the alpha1/alpha4 surface of FLIP DED1 and the alpha2/alpha5 surface of procaspase 8

231 eal previously unappreciated complexities of FLIPs, and that subtle differences within the conserved

232 differences within the conserved regions of FLIPs possess distinct molecular and structural fingerpr

233 The comparative study of FLIPs provides a unique basis to understand virus-host i

234 combined effects of androgens and FOXO3a on FLIP transcription.

235 rescue was diminished when either FOXO3a or FLIP was reduced by siRNA.

236 enerated transgenic (Tg) mice overexpressing FLIP under the CD2 promoter.

237 Similarly, cFLIPSand p22-FLIP also require TAK1 but do not require LUBAC.

238 L, cFLIPS, and their proteolytic product p22-FLIP all require the C-terminal region of NEMO/IKKgamma

239 Fluorescence loss in photobleaching (FLIP) and network analysis experiments revealed that mit

240 Fluorescence loss in photobleaching (FLIP) reveals constant retrotranslocation of WT Bax, but

241 The functional lumen imaging probe (FLIP) could improve the characterization of achalasia su

242 ithm (fatty liver inhibition of progression [FLIP]) for the classification of liver injury in morbid

243 decreased FLIP(S) ubiquitination, prolonged FLIP(S) half-life, and increased TRAIL resistance.

244 The antiapoptotic protein FLIP(S) is a key suppressor of tumor necrosis factor-rel

245 ncreases levels of the antiapoptotic protein FLIP(S), and confers resistance to tumor necrosis factor

246 e long form of the FLICE-inhibitory protein (FLIP(L)), an inhibitor of death-inducing signaling compl

247 FLICE-inhibitory protein (FLIP) blocks death receptor-mediated apoptosis by inhibi

248 The viral FLICE-like inhibitory protein (FLIP) protein from Kaposi sarcoma-associated herpesvirus

249 ting enzyme (FLICE)-like inhibitory protein (FLIP), and reduced FLIP expression precedes apoptosis af

250 DDP through a FLICE-like inhibitory protein (FLIP)-Itch interaction.

251 down-regulation of FLICE inhibitory protein (FLIP); however, the relationship between these two event

252 ced expression of the antiapoptotic proteins FLIP, Mcl-1, Bcl-2, cIAP1, cIAP2, and survivin.

253 FLICE-inhibitory proteins (FLIPs) are a family of viral (poxvirus and herpesvirus)

254 -like inhibitory protein (FLIP), and reduced FLIP expression precedes apoptosis after androgen withdr

255 ts, while in LNCaP cells, androgens regulate FLIP in a manner that is dependent on phosphoinositol-3-

256 teracting protein 4 (AIP4) pathway regulates FLIP(S) ubiquitination and stability, although the means

257 scavenger of NO, which positively regulates FLIP via S-nitrosylation.

258 ophages, FLIP long (FLIP(L)) and FLIP short (FLIP(S)) mRNA was induced by tumor necrosis factor (TNF)

259 Silencing FLIP expression significantly increased human sarcoma ce

260 These results indicate that silencing FLIP does not necessarily bypass the requirement for mit

261 on; therefore, we assessed whether silencing FLIP could convert type II cells into type I.

262 eas enforced expression of rictor stabilized FLIP(S).

263 irst evidence showing that mTORC2 stabilizes FLIP(S), hence connecting mTORC2 signaling to the regula

264 FLIP(S) steady-state levels, and suppressed FLIP(S) ubiquitination.

265 Furthermore, targeting FLIP and XIAP may represent a therapeutic strategy for t

266 These observations demonstrate that FLIP is necessary for macrophage differentiation and the

267 Here we report that FLIP has preferential affinity for the alpha1/alpha4 sur

268 Here, we show that FLIP protein expression is downregulated in castrated ra

269 The FLIP algorithm based on the SAF score should decrease in

270 In PTEN-deficient GBM cells, however, the FLIP(S) protein also exhibited a longer half-life than i

271 A FOXO3a binding site was identified in the FLIP promoter and shown necessary for the combined effec

272 ype USP8 decreased the ubiquitination of the FLIP(S) E3 ubiquitin ligase AIP4, an event previously sh

273 Equally surprising was the finding that the FLIP regions necessary for TBK1 inhibition were distinct

274 st reclassified the same slides by using the FLIP algorithm and SAF score, blinded to their first eva

275 dividuals (controls) were evaluated with the FLIP during endoscopy.

276 s able to associate with FLIP(S) or with the FLIP(S)-containing death inducing signal complex.

277 These relative affinities contribute to FLIP being recruited to the DISC at comparable levels to

278 dependent degradation of FLIP(S), leading to FLIP(S) downregulation.

279 Transgenic FLIP was expressed on CD4(+) and CD8(+) T cells and B ce

280 e results suggest that effects of transgenic FLIP on a particular autoimmune disease vary, depending

281 s a key regulator of FLIP(S) ubiquitination, FLIP(S) stability, and TRAIL sensitivity and also define

282 be detected in patients with achalasia using FLIP topography.

283 distention in patients with achalasia using FLIP topography.

284 expresses readily detectable monocistronic v-FLIP mRNAs that are undetectable in wild-type (WT) infec

285 The overexpression of v-FLIP by codon-optimized latent genomes results in a 5- t

286 ically increases the steady-state level of v-FLIP mRNA, at least in part by increasing mRNA stability

287 When codon-optimized v-FLIP sequences are reintroduced into intact KSHV genomes

288 c synergy between the latent KSHV proteins v-FLIP and v-cyclin during KSHV persistent infection that

289 cellular FLICE-inhibitory proteins (termed v-FLIP) that activates NF-kappaB and can trigger important

290 Here we show that codon usage in the v-FLIP gene is strikingly suboptimal.

291 The MC159 protein is a viral FLIP and, as such, possesses two tandem death effector d

292 The KSHV latency-associated viral FLIP (vFLIP) gene induced the expression of IL-1beta, IL

293 son of mechanistic differences between viral FLIP proteins can provide new means of precisely manipul

294 l-2 (vBcl-2) in vesicle nucleation, by viral FLIP (vFLIP) in vesicle elongation, and by K7 in vesicle

295 risingly, transgenic expression of the viral FLIP MC159 from molluscum contagiosum virus (MCV) in mic

296 Viral FLIPs (Fas-linked ICE-like protease [FLICE; caspase-8]-l

297 d state that was less able to associate with FLIP(S) or with the FLIP(S)-containing death inducing si

298 8 protein level is inversely correlated with FLIP level in vivo.

299 and patterns of contractility detected with FLIP topography may represent variations in pathophysiol

300 strated that Akt-1 physically interacts with FLIP(L).