ライフサイエンスコーパス: TRAIL

1 TRAIL continues to garner substantial interest as a reco

2 TRAIL induces cell death through binding to death recept

3 TRAIL receptor-deficient (Tnsf10 or Tr(-/-)) mice were c

4 TRAIL receptors facilitate induction of apoptosis for se

5 TRAIL regulates MID1 and TSLP, inflammation, fibrosis, s

6 TRAIL-DR-mediated ryanodine receptor activation and endo

7 TRAIL-R suppression in tumor cells impaired CCL2 product

8 five cytokine biomarkers (IL-6, IL-8, IL-10, TRAIL & IP-10), that is attributed as a sign of the body

9 elated apoptosis-inducing ligand receptor 3 (TRAIL-R3) in CSF allowed for reliable prediction of dise

10 nces in human foreskin fibroblasts and WI-38 TRAIL-resistant cells and marginally sensitive MRC-5 cel

11 central to immune networks-cluster 1 (n=58; TRAIL [tumor necrosis factor-related apoptosis-inducing

12 A TRAIL agonist that binds to human but not mouse cells in

13 We previously identified TRAILshort, a TRAIL splice variant, in HIV-infected patients and chara

14 48a is down-regulated in cells with acquired TRAIL-resistance compared with TRAIL-sensitive cells.

15 Interestingly, neutralizing antibody against TRAIL significantly reduced muXg induced OCL formation.

16 short is sufficient to protect cells against TRAIL-induced killing, whereas immunodepletion of TRAILs

17 nt of NSCLC explants with the targeted agent TRAIL revealed differential sensitivity with the majorit

18 not only DR5 transport to lysosomes but also TRAIL-induced caspase activation and apoptosis.

19 ypothesized that vitamin D deficiency alters TRAIL protein levels in human breast milk and mammary ep

20 RAIL)-induced apoptosis by the ECD, although TRAIL is still able to bind to the receptor.

21 tant UMOD were susceptible to TNF-alpha- and TRAIL-mediated apoptosis due to increased expression of

22 We conclude that CST5, AXIN1 and TRAIL are worthy of further study in the context of a pr

23 Our results identified CST5, AXIN1 and TRAIL as novel early biomarkers of TBI.

24 AXIN1 and TRAIL were able to discriminate between TBI and HV at <1

25 atory cytokines, pro-apoptotic genes BIM and TRAIL and expression of a suppressor of hepatocyte proli

26 c niche, via the recruitment of NK cells and TRAIL-dependent killing of melanoma cells by macrophages

27 hat a combination treatment of cisplatin and TRAIL would enhance cancer cell death and exhibit a "two

28 Cell growth regulation by CM and TRAIL was associated with the modulation of p53/Mdm2, Er

29 on and inducing tumour expression of Fas and TRAIL receptors.

30 ucing human transmembrane proteins, FasL and TRAIL, synthesized and displayed on oil drops induce apo

31 Evidence of both FasL and TRAIL-mediated signaling was seen after engagement of Ju

32 ects of the N-terminal gelsolin fragment and TRAIL.

33 ling an inhibitory circuit impacting PD1 and TRAIL, blocking tumor IFNG signaling promotes innate imm

34 ion of inflammatory cytokines, perforin, and TRAIL by HSPC-NK cells.

35 e demonstrate for the first time that PL and TRAIL exhibit a synergistic anti-cancer effect in cancer

36 SRC, PI3K, G-protein-coupled receptors, and TRAIL receptors.

37 study, we determined the ability of SAHA and TRAIL as single agents or in combination to inhibit the

38 that the combinatorial treatment of SAHA and TRAIL may target multiple pathways and serve as an effec

39 (SVF), TL1A was mainly expressed in SVF, and TRAIL-induced TL1A was attributed to CD4(+) and CD8(+) s

40 orts confirmed associations between TL1A and TRAIL expression in hVAT and higher leptin and IL6 serum

41 duce EoE in TRAIL-sufficient (wild-type) and TRAIL-deficient (TRAIL(-/-)) mice and targeted MID1 in t

42 d with E-selectin adhesion protein and Apo2L/TRAIL (TNF-related apoptosis-inducing ligand) apoptosis

43 In vivo, liposome-displayed Apo2L/TRAIL achieved markedly better exposure and antitumor ac

44 of its canonical extracellular ligand Apo2L/TRAIL; however, the mechanism underlying DR5 activation

45 ially enhanced cytotoxicity of soluble Apo2L/TRAIL against diverse cancer cell lines.

46 g HOTAIR in TRAIL-sensitive cells attenuated TRAIL-induced apoptosis, and shRNA-mediated HOTAIR knock

47 centration suppressed the expression of both TRAIL alpha and beta proteins.

48 TRAIL into the clinic has been confounded by TRAIL-resistant cancer populations.

49 e prostate cells sensitizes to cell death by TRAIL (TNF-related apoptosis-inducing ligand).

50 o reveal that these defenses are employed by TRAIL-expressing innate lymphoid type I cells (ILC1) but

51 ished cellular apoptotic response induced by TRAIL or the DR5 agonistic antibody AMG655 or cell killi

52 ined the role of HOTAIR in pancreatic cancer TRAIL resistance and investigated the underlying molecul

53 cancer cells, whereas in resistant cancers, TRAIL/TRAIL-R can promote metastasis via Rac1 and PI3K.

54 K (NK1.1(+)CD3(-)) cells, defined as CD49a(+)TRAIL(+)CXCR6(+)DX5(-) cells in the mouse liver, constit

55 rement of AhR for the maintenance of CD49a(+)TRAIL(+)CXCR6(+)DX5(-) liver-resident NK cells and their

56 lular microenvironment and therefore confers TRAIL resistance not only on the cell which produces it,

57 ated complex I as well as of the cytoplasmic TRAIL-induced complex II In both of these complexes, HOI

58 ificantly reduced interaction with the decoy TRAIL receptors 3 and 4.

59 -sufficient (wild-type) and TRAIL-deficient (TRAIL(-/-)) mice and targeted MID1 in the esophagus with

60 ers of magnitude superior to that of dimeric TRAIL-Fc, but also manifests more favorable pharmacokine

61 d inflammatory responses were blunted in DR5/TRAIL-R null animals.

62 ed dephosphorylation and activation of Dyn1, TRAIL-DR endocytosis, and increased resistance to TRAIL-

63 ependent on the ubiquitously expressed Dyn2, TRAIL-induced DR endocytosis is selectively regulated by

64 afenib-induced ROS accumulation that enables TRAIL to activate caspase-8 in RCC.

65 nd engineered stem cells (SC) expressing ENb-TRAIL, we show that the treatment with synthetic extrace

66 racellular matrix (sECM) encapsulated SC-ENb-TRAIL alleviates tumor burden and significantly increase

67 function and FRET studies, we show that ENb-TRAIL blocks EGFR signalling via the binding of ENb to E

68 We show that ENb-TRAIL has therapeutic efficacy in tumor cells from diffe

69 ath receptor (DR) targeted ligand TRAIL (ENb-TRAIL).

70 feres with apoptosis induction by endogenous TRAIL, which could be expressed by immune cells.

71 Collectively, endogenous TRAIL/TRAIL-R-mediated CCL2 secretion promotes accumulat

72 ur data suggest that nanoparticle-engineered TRAIL-expressing hADSCs exhibit the therapeutically rele

73 By engineering TRAIL to escape binding by DcRs, we found that DcRs do n

74 y abolished the ability of b-AP15 to enhance TRAIL- or AMG655-induced apoptosis.

75 at the N-terminal gelsolin fragment enhances TRAIL-induced loss of cell viability by inhibiting phosp

76 Herein, we examined TRAIL receptor signaling in a mouse model of cholestatic

77 unknown, however, whether and to what extent TRAIL/TRAIL-R signaling in cancer cells can affect the i

78 Finally, TRAIL and CCL2 are co-regulated with MDSC/M2 markers in

79 rly ubiquitinated targets of LUBAC following TRAIL stimulation.

80 (2020) reveal an unexpected role for TRAIL receptors in ER-stress-induced inflammation.

81 A functional inhibitory role for TRAIL-R3/4 was revealed by shRNA knockdown and mAb block

82 that TRAIL-triggered cytokine secretion from TRAIL-resistant cancer cells is FADD dependent and ident

83 Furthermore, TRAIL potentiated doxorubicin-induced decrease in beatin

84 ose inverse ex vivo correlation between hHSC TRAIL-R4 expression and susceptibility to apoptosis unde

85 Notably, despite high TRAIL expression by SG-resident ILC1, IFN-gamma producti

86 Together these results highlight TRAIL as a key ILC1-utilized effector molecule that can

87 However, TRAIL has the capacity to bind to regulatory receptors i

88 rimer-Tag) to the C-terminus of mature human TRAIL leads to a disulfide bond-linked homotrimer which

89 pite initial promise, both recombinant human TRAIL (native TRAIL) and dimeric DR4/DR5 agonist monoclo

90 However, recombinant human TRAIL demonstrates limited therapeutic efficacy in clini

91 e therapeutic potential of recombinant human TRAIL in experimental rheumatoid arthritis (RA) models.

92 asured in serum before treatment (MIG, IL22, TRAIL, APRIL, VEGF, IL3, TWEAK, SCF, IL21), identified p

93 Importantly, TRAIL-overexpressing hADSCs inhibited GBM growth, extend

94 g IFN-free therapy, suggesting a decrease in TRAIL-mediated killing by NK cells.

95 used Aspergillus fumigatus to induce EoE in TRAIL-sufficient (wild-type) and TRAIL-deficient (TRAIL(

96 n antigens to study the role of O-glycans in TRAIL-induced apoptosis.

97 Overexpressing HOTAIR in TRAIL-sensitive cells attenuated TRAIL-induced apoptosis

98 caspase-8 activation have been implicated in TRAIL-induced NF-kappaB activation; however, the underly

99 osis, and shRNA-mediated HOTAIR knockdown in TRAIL-resistant PANC-1 cells sensitized them to TRAIL-in

100 RAIL-R, a consequence of del(8p), results in TRAIL insensitivity, which may contribute to ibrutinib r

101 y epithelial cell-derived factors, including TRAIL and MID1, which promote TH 2 cell development via

102 actor superfamily (TNFSF) members, including TRAIL (TNFSF10), TL1A (TNFSF15), and their receptors, we

103 resistance to cancer therapeutics, including TRAIL, in multiresistant cancers such as RCC.

104 itionally, normal fibroblasts had incomplete TRAIL-induced caspase-8 activation compared with cancer

105 Increased TRAIL expression additionally involved the NF-kappaB and

106 ER-stress-induced TRAIL receptor activation resulted in caspase-8/FADD/RIP

107 elective targeting of the two death-inducing TRAIL receptors to maximise efficacy.

108 The potential for these inhibitory TRAIL receptors to protect hHSC from apoptosis opens new

109 The MMP12 CTD initiates TRAIL-mediated tumor cell death through its conserved SR

110 is unknown whether this was due to intrinsic TRAIL resistance within primary human cancers or insuffi

111 , as IFN-beta, IFN-gamma, IFN-lambda1, IRF7, TRAIL, and MxA expression were sustained.

112 ha-oriented side chain are superior to known TRAIL-sensitizing withanolides belonging to withaferin A

113 ation antigen CD69 and death receptor ligand TRAIL, as well as interferon-gamma (IFN-gamma) secretion

114 ENb) and death receptor (DR) targeted ligand TRAIL (ENb-TRAIL).

115 is factor-related apoptosis-inducing ligand (TRAIL) and 5-fluorouracil.

116 se to TNF-related apoptosis inducing ligand (TRAIL) and a new statistical framework for determining p

117 is factor-related apoptosis-inducing ligand (TRAIL) and by visualizing and quantifying extracellular

118 is factor-related apoptosis-inducing ligand (TRAIL) and its receptor, death receptor 4, sensitizing c

119 is factor-related apoptosis-inducing ligand (TRAIL) as drug-delivery vehicles for targeting and eradi

120 is factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in tumor cells including bre

121 f the TNF-related apoptosis-inducing ligand (TRAIL) death receptors, promoting early-phase replicatio

122 with TNF-related apoptosis-inducing ligand (TRAIL) for markedly enhanced induction of apoptosis in V

123 is factor-related apoptosis inducing ligand (TRAIL) has attracted great interest as a cancer therapy

124 is factor-related apoptosis inducing ligand (TRAIL) has been implicated in cellular growth/apoptosis,

125 is factor-related apoptosis inducing ligand (TRAIL) has been shown to increase osteoclastogenesis.

126 TNF-related apoptosis-inducing ligand (TRAIL) has been shown to induce apoptosis in malignant c

127 tor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptosis selectively via its interaction

128 is factor-related apoptosis-inducing ligand (TRAIL) is a death ligand cytokine known for its cytotoxi

129 TNF-related apoptosis-inducing ligand (TRAIL) is a death ligand that can induce apoptosis in ce

130 TNF-related apoptosis-inducing ligand (TRAIL) is a potential cancer therapy that selectively ta

131 tor (TNF)-related apoptosis-inducing ligand (TRAIL) is known for specifically killing cancer cells, w

132 is factor-related apoptosis-inducing ligand (TRAIL) or aggregation.

133 TNF-related apoptosis-inducing ligand (TRAIL) promotes inflammation through upregulation of the

134 CD95, TNF-related apoptosis-inducing ligand (TRAIL) receptors, Toll-like receptors, reactive oxygen s

135 TNF-alpha related apoptosis-inducing ligand (TRAIL) selectively kills tumor cells, without damaging n

136 The TNF-related apoptosis-inducing ligand (TRAIL) triggers apoptosis in cells by signaling through

137 TNF-related apoptosis-inducing ligand (TRAIL) was initially described to induce apoptosis of tu

138 human TNF-related apoptosis-inducing ligand (TRAIL) which induces selective apoptosis in transformed

139 is factor-related apoptosis-inducing ligand (TRAIL) with its receptor, death receptor 5 (DR5), leadin

140 is factor-related apoptosis-inducing ligand (TRAIL), a cytokine known to induce apoptosis specificall

141 ls of TNF-related apoptosis inducing ligand (TRAIL), compared with patients who failed to control HCV

142 tor (TNF)-related apoptosis-inducing ligand (TRAIL), thereby promoting viral persistence.

143 on of TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by the ECD, although TRAIL is s

144 ivate TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis have shown promising efficacy,

145 is factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in cancer cells.

146 motes TNF-related apoptosis inducing ligand (TRAIL)-induced apoptosis signal through interaction with

147 is factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, and knockdown of CAS renders c

148 uding TNF-related apoptosis-inducing ligand (TRAIL).

149 uding TNF-related apoptosis inducing ligand (TRAIL).

150 phage TNF-related apoptosis-inducing ligand (TRAIL).

151 rough TNF-related apoptosis-inducing ligand (TRAIL).

152 h the TNF-related apoptosis-inducing ligand (TRAIL).

153 TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) has long been considered a tantalizing targ

154 is factor-related apoptosis-inducing ligand (TRAIL; TNFSF10) receptor (TR) is a pro-apoptotic recepto

155 endent on receptor engagement by its ligand, TRAIL.

156 Both diffused through the endothelium, LUV-TRAIL being more efficient in killing tumour cells, show

157 ILC1 were found to be the major TRAIL expressers during both of these infection phases,

158 e that vitamin D status in mothers modulates TRAIL expression in breast milk, which may have implicat

159 hat iNSC delivery of the anticancer molecule TRAIL decreases the growth of established solid and diff

160 s, such as CD49a, and the effector molecules TRAIL and CD73.

161 vity and receptor binding kinetics as native TRAIL in vitro which are 4-5 orders of magnitude superio

162 en due to rapid systemic clearance of native TRAIL and poor apoptosis-inducing potency of dimeric ago

163 dynamic profiles in vivo than that of native TRAIL.

164 romise, both recombinant human TRAIL (native TRAIL) and dimeric DR4/DR5 agonist monoclonal antibodies

165 iable levels of TRAIL-R2/3/4 (but negligible TRAIL-R1) ex vivo and after activation.

166 counterstrategies specifically neutralizing TRAIL effector functions mediated by a specific, tissue-

167 In senescent NHCs, TRAIL-mediated apoptosis was reduced ~70%, and ETS1 dele

168 ose MSC can very efficiently vehicle a novel TRAIL variant opening unexplored opportunities for PDAC

169 ulation and ligand-independent activation of TRAIL receptors.

170 In conclusion, genetic deletion of TRAIL receptor increased the DR cell population, macroph

171 Silencing or deletion of TRAIL receptors, or their downstream effectors caspase-8

172 t-adaptive mechanism to limit the effects of TRAIL-induced cell death.

173 idence for the in vivo antitumor efficacy of TRAIL being proportional to systemic drug exposure and s

174 two cell types, their relative expression of TRAIL and gamma interferon (IFN-gamma) was assessed duri

175 bing osteoclast formation, the expression of TRAIL in human milk as a function of vitamin D status in

176 In addition, the expression of TRAIL on NK cells was reduced during IFN-free therapy, s

177 t fusion proteins in which a soluble form of TRAIL, FasL or CD40L is genetically fused to a high-affi

178 this, we evaluated two drug formulations of TRAIL (TNF-related apoptosis inducing ligand): soluble a

179 IV-1 proviral DNA, and higher frequencies of TRAIL(+) NK cells.

180 Haploinsufficiency of TRAIL-R, a consequence of del(8p), results in TRAIL inse

181 Therefore, inhibition of TRAIL expression could be an effective countermeasure fo

182 mutagenesis to prove that the inhibition of TRAIL-induced apoptosis by the ECD predominantly comes f

183 Repetitive injection of TRAIL-overexpressing hADSCs significantly prolonged anim

184 in D deficient mothers showed high levels of TRAIL (alpha and beta) proteins compared to milk from vi

185 ) was performed to investigate the levels of TRAIL DR4, DR5 and OPG receptors generating promising in

186 y screening that muXg induces high levels of TRAIL expression in murine preosteoclast cells in the ab

187 ifferent donors expressed variable levels of TRAIL-R2/3/4 (but negligible TRAIL-R1) ex vivo and after

188 4, sensitizing cells to an autocrine loop of TRAIL-mediated cell death.

189 The apoptotic potential of TRAIL-R2 on hHSC was confirmed by lentiviral-mediated kn

190 amino acid residues 1-70) in the presence of TRAIL impairs cell viability of TRAIL resistant transfor

191 reased IL-6 levels, suppressed production of TRAIL, and reduced infiltration of polymorphonuclear cel

192 transfection led to robust up-regulation of TRAIL in hADSCs, and that TRAIL-expressing hADSCs induce

193 ere IFNalpha induces macrophage secretion of TRAIL that causes endocytosis of Na,K-ATPase by the alve

194 f recent preclinical and clinical studies of TRAIL-induced apoptosis, and current attempts to overcom

195 for cancer therapeutics, the translation of TRAIL into the clinic has been confounded by TRAIL-resis

196 presence of TRAIL impairs cell viability of TRAIL resistant transformed human hepatocytes (HepG2).

197 sis of hHSC in response to both oligomerised TRAIL and NK cells.

198 L- or DR5-mediated anticancer therapy and on TRAIL/DR5-mediated immune-clearance of cancer cells.

199 ults support a causative effect of HOTAIR on TRAIL sensitivity.

200 egative impact of B-Raf or MEK inhibition on TRAIL- or DR5-mediated anticancer therapy and on TRAIL/D

201 ligands TNF-alpha (Tumor Necrosis Factor) or TRAIL (TNF-Related Apoptosis-Inducing Ligand); is an ext

202 determined the different effects of SAHA or TRAIL alone and combining SAHA with TRAIL on the express

203 nstrate that the distinct effects of SAHA or TRAIL individually and in combination on the proliferati

204 lar mechanisms may facilitate either SAHA or TRAIL targeted use and the selection of suitable combina

205 lines to cell death by agonists TNFalpha or TRAIL and inhibited cIAP1>XIAP>IAP2.

206 unction may represent a strategy to overcome TRAIL resistance in pancreatic cancer.

207 apoptosis, and current attempts to overcome TRAIL resistance, and we provide a perspective for impro

208 Here we demonstrate that sorafenib overcomes TRAIL resistance in RCC by a mechanism that does not rel

209 el paradigm for understanding and overcoming TRAIL resistance, in particular how HIV-infected cells e

210 on of innate immune cells, including a PD1(+)TRAIL(+) ILC1 population.

211 dministering a potent, long-acting PEGylated TRAIL (TRAILPEG) is profoundly anti-rheumatic against tw

212 Contrary to its role in preventing TRAIL-induced RIPK1-independent apoptosis, HOIP presence

213 KK complex to complex I, LUBAC also promotes TRAIL-induced activation of NF-kappaB and, consequently,

214 tes as a carrier for the anti-cancer protein TRAIL could be an effective tool to directly target circ

215 firmed our hypothesis that membrane-proximal TRAIL species lack the capacity to physically engage the

216 ed apoptosis-inducing ligand-death receptor (TRAIL-DR) complexes in several cancer cells.

217 nt agonistic activity of the TRAIL-receptor (TRAIL-R)-targeting drugs.

218 d apoptosis-inducing ligand death receptors (TRAIL-DR), we show that TRAIL-DR signaling significantly

219 al roles for the regulatory TRAIL receptors (TRAIL-R3/4) in a physiological setting.

220 Here, we show that DcRs also regulate TRAIL sensitivity at a supracellular level and thus repr

221 Consistently, vitamin D regulated TRAIL mRNA expression in HME-1 cells.

222 ave dissected the contribution of regulatory TRAIL receptors to apoptosis resistance in primary human

223 edundant functional roles for the regulatory TRAIL receptors (TRAIL-R3/4) in a physiological setting.

224 on of TRAILshort with a specific Ab restores TRAIL sensitivity.

225 LKL-containing complex, LUBAC also restricts TRAIL-induced necroptosis.

226 The resulting TRAIL-Trimer not only retains similar bioactivity and re

227 3-36 and compared their ability to sensitize TRAIL-mediated apoptosis in a panel of renal carcinoma c

228 ecently developed the genetically stabilized TRAIL platform TR3 in efforts to improve the limitations

229 We propose that, upon ER stress, TRAIL receptors serve as "stress-associated molecular pa

230 being a dominant negative ligand to subvert TRAIL-mediated killing.

231 n of RNF183 expression was found to suppress TRAIL-induced activation of caspase-8 and caspase-3.

232 t up-regulation of TRAIL in hADSCs, and that TRAIL-expressing hADSCs induced tumor-specific apoptosis

233 We find that TRAIL induces up-regulation of CAS in a posttranscriptio

234 We hypothesize that TRAIL may play an important role in muXg enhanced OCL di

235 These results indicate that TRAIL signaling plays an important role in the muXg incr

236 We observed that TRAIL-resistant pancreatic cancer cells had higher level

237 We show that TRAIL stimulation activates ryanodine receptor-mediated

238 and death receptors (TRAIL-DR), we show that TRAIL-DR signaling significantly restricts both early an

239 Here we show that TRAIL-triggered cytokine secretion from TRAIL-resistant

240 The TRAIL pathway can mediate apoptosis of hepatic stellate

241 The TRAIL-expressing platelets were demonstrated to kill can

242 ominant negative ligand that antagonizes the TRAIL-dependent pathway of cell death, which we called T

243 Because the TRAIL pathway has been implicated in CD4 T cell death oc

244 i-CSC effect is significantly blocked by the TRAIL sequestering antibody RIK-2.

245 s by blocking activation of caspase-8 by the TRAIL-R2/DR5 death receptor; notably, this activation wa

246 ected cells escape immune elimination by the TRAIL:TRAILshort receptor axis.

247 Hence, LUBAC controls the TRAIL signalling outcome from complex I and II, two plat

248 cer cells is FADD dependent and identify the TRAIL-induced secretome to drive monocyte polarization t

249 ls (0.5 to 5 nM) significantly increased the TRAIL alpha but no change in beta expression.

250 g protein, mediates cell death involving the TRAIL receptors in the hepatic stellate cell line, LX2.

251 R expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR kn

252 Inhibition of the TRAIL signaling pathway has been shown to improve lung i

253 Here, we show that LUBAC forms part of the TRAIL-R-associated complex I as well as of the cytoplasm

254 rs or insufficient agonistic activity of the TRAIL-receptor (TRAIL-R)-targeting drugs.

255 mor-supportive immune-modulatory role of the TRAIL/TRAIL-R system in cancer biology.

256 Thus, the TRAIL pathway plays a critical role in tissue remodeling

257 Its gene therapy with the TRAIL suicide gene effectively induces apoptosis of HeLa

258 7 cells in inflamed arthritic joints through TRAIL-induced apoptosis while increasing anti-inflammato

259 ceptor signaling through FADD and TNFRSF10B (TRAIL-R2) as a key mediator of CAR T-cell cytotoxicity a

260 ion of ILC-associated IL7R (CD127), TNFSF10 (TRAIL), KIT (CD117), IL2RA (CD25), CD27, CXCR3, DPP4 (CD

261 ystem to regulate the expression of TNFSF10 (TRAIL) in the context of glioma therapy and found that i

262 the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5

263 has been shown to sensitize cancer cells to TRAIL-induced apoptosis, in particular by down-regulatio

264 appaB and AP-1 sites and sensitized cells to TRAIL-induced apoptosis.

265 ic compounds for sensitizers of RCC cells to TRAIL-mediated apoptosis led to identification of the 17

266 efficacy in clinical trials, possibly due to TRAIL-resistance of primary cancers and its inherent sho

267 ctivity and sensitized normal fibroblasts to TRAIL-mediated apoptosis.

268 show that TRAILshort binds preferentially to TRAIL receptors 1 and 2 with significantly reduced inter

269 modified to enhance sensitization of RCCs to TRAIL-mediated apoptosis, thereby assisting development

270 -DR endocytosis, and increased resistance to TRAIL-induced apoptosis.

271 egulation of caspase-8 confers resistance to TRAIL-induced cell death in normal cells through blockad

272 g TRAIL-mediated apoptosis and resistance to TRAIL.

273 e cancer cells have developed resistances to TRAIL which limits anticancer potential.

274 but many pancreatic cancers are resistant to TRAIL therapy.

275 ne MCs from wild-type mice were resistant to TRAIL-induced apoptosis, SCF-stimulated MCs underwent ap

276 knockdown of CAS renders cells resistant to TRAIL.

277 , including lung cancer, remain resistant to TRAIL.

278 lated MCs underwent apoptosis in response to TRAIL.

279 ended O-glycans and become more sensitive to TRAIL treatment.

280 tumor cells attenuates their sensitivity to TRAIL treatment; when transfected with wild-type Cosmc,

281 eptors (DR4 and DR5), but the sensitivity to TRAIL-induced apoptosis of cells varies, and the attribu

282 n also resulted in greater susceptibility to TRAIL-induced cell death, consistent with its proapoptot

283 IL-resistant PANC-1 cells sensitized them to TRAIL-induced apoptosis.

284 d cancer cells to PLX4032 sensitizes them to TRAIL-induced apoptosis; this is also a c-Raf/MEK/ERK-de

285 ich the microenvironment can diminish tumour TRAIL sensitivity.

286 ss different molecular mechanisms underlying TRAIL-mediated apoptosis and resistance to TRAIL.

287 Instead CXCR6+ NK could upregulate TRAIL, a key death ligand in hepatitis pathogenesis.

288 s (PBMCs) from patients with SVR upregulated TRAIL, as well as IFN-gamma and the chemokines CXCL9 and

289 that it is ILC1 that curtail replication via TRAIL in the absence of m166-imposed countermeasures.

290 higher levels of HOTAIR expression, whereas TRAIL-sensitive pancreatic cancer cells had lower HOTAIR

291 receptors, were enriched in E2F1(high) While TRAIL was equally expressed in adipocytes and stromal va

292 lin peptide1-70 alone or in combination with TRAIL, induced inhibition of Akt phosphorylation and key

293 ively augmented apoptosis when combined with TRAIL or the DR5 agonistic antibody AMG655; these effect

294 with acquired TRAIL-resistance compared with TRAIL-sensitive cells.

295 rginally sensitive MRC-5 cells compared with TRAIL-sensitive human lung and colon cancer cells.

296 mechanisms of combining HDAC inhibitors with TRAIL in the treatment of breast cancer are poorly under

297 SAHA or TRAIL alone and combining SAHA with TRAIL on the expression of a number of apoptosis-related

298 re, we reasoned that PL would synergize with TRAIL to stimulate potent apoptosis in cancer cells.

299 ompared with C4-2-DN cells when treated with TRAIL-TZD, thus suggesting that C4-2-DN cells were more

300 e revealed that the key factors (e.g. WNT5A, TRAIL, CSF1, etc.) mediated the activation of PC-Treg an