ライフサイエンスコーパス: death ligand

1 er several days of culture in the absence of death ligand.

2 astoma cells to apoptosis induced by various death ligands.

3 side more proximal in the pathway serving as death ligands.

4 r FADD in sensitization to IAP inhibitor and death ligands.

5 death 1 (anti-PD-1) and anti-programmed cell death ligand 1 (anti-PD-L1 ) therapy for treatment of lu

6 costimulation but is dependent on programmed death ligand 1 (B7-H1).

7 t programmed cell death protein 1/programmed death ligand 1 (PD-1/PD-L1) and cytotoxic T lymphocyte-a

8 , particularly programmed death 1/programmed death ligand 1 (PD-1/PD-L1) blockade, have improved the

9 ctions via the programmed death 1/programmed death ligand 1 (PD-1/PD-L1) pathway down-regulate immune

10 ory checkpoint blockade with anti-programmed death ligand 1 (PD-L1) Ab can restore functions to exhau

11 The approval of anti-programmed death ligand 1 (PD-L1) and anti-programmed death 1 agent

12 We examined the expression of Programmed Death Ligand 1 (PD-L1) and defined the tumor immune micr

13 These cells also express programmed death ligand 1 (PD-L1) and interleukin-10, and directly

14 Blocking the interaction between Programmed Death Ligand 1 (PD-L1) and its receptor, PD-1, is an eff

15 hat block the interaction between programmed death ligand 1 (PD-L1) and PD-1 have shown impressive an

16 ced solid tumours expressing programmed cell death ligand 1 (PD-L1) and report here on the interim an

17 The anti-programmed death ligand 1 (PD-L1) antibody atezolizumab is clinical

18 and in subgroups on the basis of programmed death ligand 1 (PD-L1) expression and human papillomavir

19 hibitors has been associated with programmed death ligand 1 (PD-L1) expression levels in several canc

20 We found increased programmed death ligand 1 (PD-L1) expression on F4/80 macrophages,

21 Here we show that programmed death ligand 1 (PD-L1) expression on tumor cells can ren

22 K /ROS1), if the patient has high programmed death ligand 1 (PD-L1) expression, pembrolizumab should

23 et that required interaction with programmed death ligand 1 (PD-L1) for development.

24 acquire the coinhibitory molecule programmed death ligand 1 (PD-L1) from mature dendritic cells (mDC)

25 mmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) have shown remarkable activity in

26 ng the programmed death 1 (PD-1): programmed death ligand 1 (PD-L1) immune checkpoint in lung cancer,

27 T cells upregulated expression of programmed death ligand 1 (PD-L1) in a signal transducer and activa

28 lymphocyte antigen 4 (CTLA-4) and programmed death ligand 1 (PD-L1) in an established murine transgen

29 ogrammed cell death protein 1 and programmed death ligand 1 (PD-L1) inhibitors to docetaxel, the curr

30 Programmed death ligand 1 (PD-L1) is an immune regulatory ligand th

31 Programmed death ligand 1 (PD-L1) is expressed by multiple tumors,

32 Programmed death ligand 1 (PD-L1) is expressed on a number of immun

33 Programmed cell death ligand 1 (PD-L1) is part of an immune checkpoint s

34 r, virus-induced dysregulation of programmed death ligand 1 (PD-L1) may play a role.

35 The programmed cell death ligand 1 (PD-L1) participates in an immune checkpo

36 ibitory programmed death 1 (PD-1)-programmed death ligand 1 (PD-L1) pathway contributes to the functi

37 cell death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1) pathway is a negative regulator o

38 ation was stratified according to programmed death ligand 1 (PD-L1) status, BRAF mutation status, and

39 Administration (FDA) detect programmed cell death ligand 1 (PD-L1) to enrich for patient response to

40 found a higher frequency of programmed cell death ligand 1 (PD-L1)(+) germinal center B cells from l

41 e negative costimulatory molecule programmed death ligand 1 (PD-L1), and HSCs extracted from wild-typ

42 express the ligand for PD-1, programmed cell death ligand 1 (PD-L1), facilitating their escape from t

43 te lower expression of inhibitory programmed death ligand 1 (PD-L1), HMPV-specific CD8(+) T cells of

44 ntibody that binds selectively to programmed death ligand 1 (PD-L1), in this patient population.

45 ors of T-cell activation, such as programmed death ligand 1 (PD-L1), programmed death 1 ligand 2 (PD-

46 ress IgA, interleukin (IL)-10 and programmed death ligand 1 (PD-L1), the appearance of which depends

47 s, such as the expression of programmed cell death ligand 1 (PD-L1), the inhibition of which results

48 raction with the B7 family member programmed death ligand 1 (PD-L1), which is substantially expressed

49 ith chemotherapy in patients with programmed death ligand 1 (PD-L1)-positive NSCLC.

50 d and neck cancers (HNC), express programmed death ligand 1 (PD-L1).

51 s defined by status regarding the programmed death ligand 1 (PD-L1).

52 ured and fetal liver HSCs express programmed death ligand 1 (PD-L1).

53 Recently, agents targeting the programmed death ligand 1 (PD-L1)/programmed death receptor 1 (PD-1

54 Programmed death ligand 1 (PD-L1, also known as B7 homolog 1 or CD2

55 rein, we investigated the role of programmed death ligand 1 (PDL-1) in T cell priming and immunity co

56 ry T cell costimulatory molecule, programmed death ligand 1 (PDL1), has an important role in conferri

57 The programmed death ligand 1 (PDL1)/programmed death 1 (PD1) costimula

58 Programmed death ligand 1 (PDL1, or B7-H1) is expressed constitutiv

59 antigen 4 (CTLA-4/CD152) and programmed cell death ligand 1 (PDL1/CD274) showed clinical efficacy in

60 therapy with anti-CTLA-4 and anti-programmed death ligand 1 Abs, even when checkpoint blockade alone

61 Blockade of programmed death ligand 1 and 2, but not CD40, TGF-beta signaling,

62 ependent upon the balance between programmed death ligand 1 and IL-12 expression.

63 Blocking the programmed death ligand 1 binding site just before i.v. injection o

64 and sensitize tumors to PD-1/programmed cell death ligand 1 blockade-induced rejection.

65 s largely unaffected by PD-1/programmed cell death ligand 1 blockade.

66 ly, these LP DCs upregulated programmed cell death ligand 1 during the initial interaction with MOG-s

67 100; P < .001) and increased programmed cell death ligand 1 expression (0 vs 1.5; P < .001) in the im

68 by tumor-infiltrating T cells and programmed death ligand 1 expression in the prostate, disrupting pr

69 P3C stimulation did not induce programmed death ligand 1 expression on LSECs, thereby favoring T c

70 te/proinflammatory, and increased programmed death ligand 1 expression on natural killer cells (incre

71 te, disrupting programmed death 1/programmed death ligand 1 interaction did not enhance T cell functi

72 of ICOS or the programmed death-1/programmed death ligand 1 pathway was shown to abolish the regulati

73 ntact programmed death 1 receptor-programmed death ligand 1 signaling pathway and CD4(+)CD25(+)Foxp3(

74 inally, programed death protein 1/programmed death ligand 1 signaling pathways were essential in pote

75 ession of the inhibitory molecule programmed death ligand 1 that, through interaction with programmed

76 Tfh cells consistently expressed programmed death ligand 1 upon activation.

77 lation of OX40 ligand (OX40L) and programmed death ligand 1(PD-L1) expression.

78 PD-L1 (programmed death ligand 1) and PD-L2 are cell-surface glycoproteins

79 examined the role of B7-H1 (programmed cell death ligand 1) in resistance to primary Salmonella infe

80 ng PD-1/PD-L1 (programmed death-1/programmed death ligand 1) interactions-is showing impressive clini

81 oxic T-lymphocyte antigen 4, anti-programmed death ligand 1) or proinflammatory cytokines (interleuki

82 en, express high levels of PDL-1 (programmed death ligand 1), and are more efficient than Ly6C(high)

83 such as programmed death 1 (PD1)/programmed death ligand 1, leading to T cell exhaustion and providi

84 n, such as the B7 family molecule programmed death ligand 1, was upregulated upon activation of T cel

85 tly, expression of the inhibitory programmed death ligand 1, which was up-regulated on FRC after infe

86 Conclusion In patients with programmed death ligand 1-positive advanced cervical cancer, pembro

87 d efficacy of pembrolizumab in 20 programmed death ligand 1-positive, advanced solid tumor cohorts.

88 duces Treg expression of CD39 and programmed death ligand 1.

89 expression of programmed death 1/programmed death ligand 1.

90 tact-dependent manner mediated by programmed death ligand 1.

91 ional FOXP3(+) Treg cells through programmed death ligand 1.

92 an leukocyte antigen class II and programmed death ligand 1.

93 eukocyte antigen-DR (HLA-DR), and programmed death ligand 1/2 (PDL1/2) measured on pDCs.

94 -ligand 2 (B7-DC; CD273), whereas programmed death-ligand 1 (B7-H1; CD274) and inducible costimulator

95 To investigate the expression of programmed death-ligand 1 (PD-L1) and immune checkpoints and their

96 Programmed death-ligand 1 (PD-L1) and PD-L2 are B7 family members e

97 olizumab (MPDL3280A), a humanized programmed death-ligand 1 (PD-L1) antibody, in renal cell carcinoma

98 hanced when combined with an anti-programmed death-ligand 1 (PD-L1) antibody.

99 Durable tumor immunity required programmed death-ligand 1 (PD-L1) blockade in combination with an a

100 that influence responsiveness to programmed death-ligand 1 (PD-L1) blockade.

101 Programmed death-ligand 1 (PD-L1) down-modulates various immune res

102 ibody blockade of either IL-10 or programmed death-ligand 1 (PD-L1) during viral persistence enhances

103 ory mechanism is up-regulation of programmed death-ligand 1 (PD-L1) expressed on tumor or stromal cel

104 evaluated the prognostic value of programmed death-ligand 1 (PD-L1) expression in CTCs in colorectal

105 he immune suppression mediated by programmed death-ligand 1 (PD-L1) expression on cancer cells accomp

106 asive immuno-PET imaging of human programmed death-ligand 1 (PD-L1) expression, in a preclinical mode

107 umor-infiltrating lymphocytes and programmed death-ligand 1 (PD-L1) expression.

108 y of avelumab, a fully human anti-programmed death-ligand 1 (PD-L1) IgG1 antibody, in patients with r

109 he programmed cell death 1 (PD-1)/programmed death-ligand 1 (PD-L1) immune checkpoint augments antitu

110 d a heterogeneous distribution of programmed death-ligand 1 (PD-L1) in Her2 transgenic mouse mammary

111 f Toll-like receptor 2 (TLR2) and programmed death-ligand 1 (PD-L1) in regulating alpha-(1,3)-glucan-

112 We hypothesize the programmed death-ligand 1 (PD-L1) inhibitor, durvalumab, olaparib,

113 Purpose Expression of programmed death-ligand 1 (PD-L1) is a potential predictive marker

114 Atezolizumab is a humanised antiprogrammed death-ligand 1 (PD-L1) monoclonal antibody that inhibits

115 the ICPs analyzed, expression of programmed death-ligand 1 (PD-L1) on tumor and infiltrating T cells

116 Deficiencies in the PD-1/programmed death-ligand 1 (PD-L1) pathway are associated with autoi

117 d cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) pathway play an important immunos

118 ombining MEK inhibition with anti-programmed death-ligand 1 (PD-L1) resulted in synergistic and durab

119 l lung cancer (NSCLC) with a programmed cell death-ligand 1 (PD-L1) tumour proportion score of 50% or

120 NA-mediated induced expression of Programmed Death-Ligand 1 (PD-L1) which inhibits T-cell proliferati

121 Inhibition of programmed death-ligand 1 (PD-L1) with atezolizumab can induce dura

122 arkedly reduced the expression of programmed death-ligand 1 (PD-L1), a negative regulator of cytotoxi

123 ammed cell death protein 1 (PD1), programmed death-ligand 1 (PD-L1), and B and T lymphocyte attenuato

124 cells (HSCs) suppress T cells via programmed death-ligand 1 (PD-L1), but it remains unknown whether t

125 nd blocking its canonical ligand, programmed death-ligand 1 (PD-L1), lengthened the duration of migra

126 ction of cytokines, expression of programmed death-ligand 1 (PD-L1), secretion of type 1 interferons

127 Programmed death-ligand 1 (PD-L1), which exerts T cell suppression

128 illance via stabilization of programmed cell death-ligand 1 (PD-L1).

129 of the T cell negative regulator programmed death-ligand 1 (PD-L1, also called B7-H1) can enhance T

130 Programmed death-ligand 1 (PD-L1; also called B7-H1 or CD274), whic

131 ication through the expression of programmed death-ligand 1 (PD-L1; also called CD274 or B7-H1) in th

132 roves the therapeutic efficacy of programmed death-ligand 1 (PD-L1; also known as B7-H1) checkpoint b

133 study assessed atezolizumab (anti-programmed death-ligand 1 [PD-L1]) as treatment for metastatic urot

134 nd efficacy of atezolizumab (anti-programmed death-ligand 1 [PD-L1]) versus chemotherapy in this pati

135 dity, and decreased expression of programmed death-ligand 1 and induction of Tregs.

136 Programmed death-ligand 1 expression on tumor cells and ICs, PD-L1

137 thods Patients were stratified by programmed death-ligand 1 expression, BRAF status, and best prior c

138 r programmed cell death protein 1/programmed death-ligand 1 have displayed durable clinical responses

139 mmunization induced expression of programmed death-ligand 1 in the tumor lesions.

140 In return, programmed death-ligand 1 interacts with the constitutively express

141 istration induces upregulation of programmed death-ligand 1 on dendritic cells in a T cell-dependent

142 , but not those of CD80, CD86, or programmed death-ligand 1 or 2, correlated with T cell responsivene

143 y blocking programmed death-1 and programmed death-ligand 1 pathway in vitro and in vivo, resulting i

144 Tumor size and programmed death-ligand 1 status were among the baseline factors in

145 h cannot recognize peptidoglycan, programmed death-ligand 1 was undetected.

146 ne tolerance-associated molecule 'programmed death-ligand 1', whereas in NOD1/2 double knockout mice,

147 ssion of immune modulators PD-L1 (programmed death-ligand 1) and CD86 by myeloid DCs (mDCs) and decre

148 ion levels of the CD274 molecule (programmed death-ligand 1) and programmed cell death 1, markers of

149 adaptive immune checkpoint PD-L1 (programmed death-ligand 1).

150 tory pathways in T cells, such as programmed death-ligand 1, programmed cell death 1, or transforming

151 cells and enhanced expression of programmed death-ligand 1, whose expression on monocytes and dendri

152 IgM expression (67%), and lack of programmed death-ligand 1/ligand 2.

153 but comparatively high levels of programmed death ligand-1 (B7-H1), and were resistant to pro-inflam

154 tanding of the programmed death-1/programmed death ligand-1 (PD-1/PD-L1) pathway (referred to as the

155 impairment via programmed death-1/programmed death ligand-1 (PD-1/PD-L1) signaling, a pathway previou

156 naling through programmed death-1/programmed death ligand-1 (PD-1/PD-L1), but not through cytotoxic T

157 Signaling via programmed death ligand-1 (PD-L1) and PD-L2 is crucial for maintain

158 Extracellular interaction between programmed death ligand-1 (PD-L1) and programmed cell death protein

159 ammed cell death protein-1 (PD-1)/programmed death ligand-1 (PD-L1) checkpoint blockade has led to re

160 ession of the coinhibitory ligand programmed death ligand-1 (PD-L1) concurrent with enrichment of the

161 IFN-gamma is a critical driver of programmed death ligand-1 (PD-L1) expression in cancer and host cel

162 Programmed death ligand-1 (PD-L1) interaction with PD-1 induces T c

163 Programmed death ligand-1 (PD-L1) interacts with programmed death-1

164 Programmed death ligand-1 (PD-L1) is a critical regulator of T cell

165 a negative costimulatory molecule programmed death ligand-1 (PD-L1) is defective in SLE patients with

166 Programmed cell death ligand-1 (PD-L1) is typically produced by cancer c

167 an inhibitory programmed death-1-programmed death ligand-1 (PD-L1) pathway occurs in several chronic

168 of the programmed death-1 (PD-1)-programmed death ligand-1 (PD-L1) pathway, a major pathway known to

169 via the programmed death-1 (PD-1)-programmed death ligand-1 (PD-L1) pathway.

170 Programmed death ligand-1 (PD-L1) plays a critical role in T-cell r

171 eat biopsy for assessment of programmed cell death ligand-1 (PD-L1) status.

172 between PD-1 and its ligand programmed cell death ligand-1 (PD-L1) with monoclonal antibodies has sh

173 homolog 1 (B7-H1), also known as programmed death ligand-1 (PD-L1), is increased in many pathologica

174 population exhibiting the markers programmed death ligand-1 (PD-L1), Mac-2, and macrophage mannose re

175 this model, loss of PD-1, but not programmed death ligand-1 (PD-L1), on the antigen-specific CD4(+) T

176 e negative costimulatory molecule programmed death ligand-1 (PD-L1), while commensurately down-regula

177 e immune inhibitory molecule programmed cell death ligand-1 (PD-L1; also known as B7-H1), in a manner

178 yeloid DC between the groups, the programmed death ligand-1 (PD-L1=B7-H1):CD86 (B7-2) ratio on precur

179 uring persistent viral infection, programmed death ligand-1 (PDL-1) also stimulates the expansion of

180 unity through their expression of programmed death ligand-1 (PDL1 or B7-H1), which interacts with T c

181 but they did express higher programmed cell death ligand-1 (PDL1) than other neutrophils, and lympho

182 f the immune checkpoint inhibitor programmed death ligand-1 and accumulation of T-regulatory cells an

183 sulted in increased expression of programmed death ligand-1 and the production of increased amounts o

184 , our data suggest that PD-1/programmed cell death ligand-1 blockade using soluble rPD-1-Fc instead o

185 e, whereas programmed death-1 and programmed death ligand-1 expression were upregulated in activated

186 were achieved regardless of tumor programmed death ligand-1 expression.

187 rvival (OS) and response by tumor programmed death ligand-1 expression.

188 ogrammed cell death-1 (PD-1)/programmed cell death ligand-1 pathway has been shown to limit cell-medi

189 riments, antibody blockade of the programmed death ligand-1 receptor programmed death receptor-1 (PD-

190 was, in contrast to inhibition by programmed death ligand-1-Fc, not overcome by anti-CD28 costimulati

191 n molecules CD80, CD83, CD40, and programmed death ligand-1.

192 therapy but not with anti-PD-1 or programmed death ligand-1.

193 D-1:PDL1/PDL2 (programmed death-1:programmed death ligand-1/2) plays an important role in regulating

194 -1 and up-regulated expression of programmed death ligands-1 and 2 after activation.

195 s varying in capacity to override programmed death-ligand-1 inhibitory effects contributes to the res

196 We report that programmed death ligand 2 (PD-L2), a known ligand of PD-1, also bin

197 of CD5+ B-1 cells that expressed programmed death ligand 2 (termed L2pB1 cells).

198 members (CD80, CD86, ICOS-L, and programmed death ligand 2 [PD-L2]) were not expressed on class II(+

199 moting IFN regulatory factor 4(+) programmed death ligand 2(+) dendritic cells and ILT3(+) rebounded

200 CII(hi) DC revealed expression of programmed death ligand 2, CD301b, IFN regulatory factor 4, and mod

201 luding IL-10, TGF-beta1, IDO, and programmed death ligand 2, T. cruzi infection induced an early incr

202 C class II, CD40, CD80, CD86, and programmed death-ligand 2 (B7-DC; CD273), whereas programmed death-

203 ce expression of CD11c, CD73, and programmed death-ligand 2.

204 (i) the death receptor pathway activated by death ligands and (ii) the DNA damage pathway activated

205 ntly reduced messenger RNA (mRNA) levels for death ligands and death receptors in hepatocytes, as wel

206 eficient Jurkat cells, to assess whether the death ligands and gangliosides overexpressed by the rena

207 elevated apoptosis/programmed cell death and death ligands and their receptors in the pathogenesis of

208 s ligand (FasL) belongs to the TNF family of death ligands, and its binding to the FasR leads to acti

209 activities and increased sensitivity to the death ligand Apo-2 ligand/tumor necrosis factor-related

210 taxane antimicrotubule agent, as well as the death ligand Apo-2L/TRAIL (tumor necrosis factor-alpha-r

211 TNF superfamily death ligands are expressed on the surface of immune cel

212 sed cells in vivo, spurring interest in this death ligand as a potential therapeutic.

213 lated apoptosis-inducing ligand (TRAIL) is a death ligand cytokine known for its cytotoxic activity a

214 P-dependent death program often initiated by death ligand/death receptor interactions, such as Fas li

215 related apoptosis-inducing ligand (TRAIL), a death ligand expressed by cells of the innate immune sys

216 ce death receptors, which respond to cognate death ligands expressed on immune-effector cells.

217 totic body-"fed" Kupffer cells with enhanced death ligand expression; inhibition of hepatocyte apopto

218 hepatic NK cells, surface expression of the death ligand FasL, and capacity to kill FasL-sensitive t

219 and favors a model in which BID represents a death ligand for the membrane-bound receptor BAX.

220 Both apoptotic body phagocytosis and death ligand generation were attenuated by gadolinium ch

221 ecently, other biological functions of these death ligands have been postulated in vitro and in vivo.

222 tead CXCR6+ NK could upregulate TRAIL, a key death ligand in hepatitis pathogenesis.

223 e that tBID functions as a membrane-targeted death ligand in which an intact BH3 domain is required f

224 further enhanced by physiologically relevant death ligands including TNF-related apoptosis inducing l

225 beads, stimulated Kupffer cell generation of death ligands, including Fas ligand, and tumor necrosis

226 Despite the known role of FADD in mediating death-ligand induced apoptosis, neutralizing antibodies

227 b increased TRAIL-induced Bak activation and death ligand-induced apoptosis in a wide variety of neop

228 indicating that colchicine protects against death ligand-induced apoptosis in the liver by decreasin

229 8 activities, indicating that IRF-1 mediates death ligand-induced hepatocyte death.

230 ibody-mediated disruption of PD-1/programmed death ligand interaction.

231 We have termed this protein TNF-related death ligand-la (TRDL-1alpha).

232 ific differences in the endogenous levels of death ligands may apply different selective pressures on

233 lls were efficiently lysed by NK cells using death ligand-mediated apoptosis.

234 This death ligand-mediated killing did not depend on NKG2D re

235 naling in NK cells required for perforin and death ligand-mediated lysis of tumor target cell are qui

236 Death ligands of the Tumor Necrosis Factor (TNF) family

237 mulatory molecules of DCs such as programmed death ligands, OX40 ligand, and inducible T-cell costimu

238 Moreover, we have identified programmed cell death ligand (PD-L) 2 as a negative regulator of TH9 cel

239 in IL-10 and higher expression of programmed death ligand (PD-L)1 and PD-L2 - which were partially de

240 on the programmed death 1 (PD-1)-programmed death ligand (PD-L)1 pathway, not the distinct cytotoxic

241 FN)-gamma, programed death (PD)-1, programed death ligand (PD-L)1, and the suppression of hepatitis B

242 ulatory molecules, including programmed cell death ligand (PD-L)1, PD-L2, CD40, CD80, CD86, and induc

243 timulatory molecules, such as the programmed death ligand (PD-L1), might exert differential effects o

244 Programmed death ligands (PD-Ls) on antigen-presenting cells intera

245 Programmed death-ligand (PD-L)1 and PD-L2, newer B7 superfamily mem

246 We studied program death-ligand (PD-L)1 in neurons and gliomas in tumors fr

247 romoting the tolerogenic markers, programmed death-ligand (PD-L)1, PD-L2, and the tryptophan degradin

248 dization here, we report that the programmed death ligand (PDL) locus (9p24.1) is frequently and spec

249 Programmed death ligands (PDLs) are immune-regulatory molecules tha

250 Because Mincle can ligate the cell death ligand SAP130, we postulated that Mincle signaling

251 dentical to drug-naive cells with respect to death ligand sensitivity and gene expression profiles.

252 bset of cells from induction of apoptosis by death ligands such as Fas ligand and tumor necrosis fact

253 In particular, death ligands such as tumour necrosis factor (TNF)-alpha

254 lated apoptosis-inducing ligand (TRAIL) is a death ligand that can induce apoptosis in cells expressi

255 TRAIL is a recently isolated death ligand that possesses selective anti-tumor activit

256 related apoptosis-inducing ligand (TRAIL), a death ligand that, failing to kill CCA cells, instead pr

257 ) cytotoxic T lymphocytes and killing by the death ligands TNF, Fas ligand and TRAIL.

258 rcinoma cells to various drugs, ranging from death ligands to endoplasmic reticulum stress.

259 e required for apoptosis induced by the cell death ligand TRAIL (TNF-related apoptosis-inducing ligan

260 The cytotoxic death ligand TRAIL (tumor necrosis factor-related apopto

261 ature NK cells constitutively expressing the death ligand TRAIL depended on T-bet.

262 From this data we conclude the death ligand TRAIL preferentially provokes apoptosis of

263 The ability of the death ligand TRAIL to induce tumor cell apoptosis has le

264 The death ligand, TRAIL (tumor necrosis factor-related apopt

265 or a novel therapeutic strategy in which the death ligand, TRAIL, is safely combined with conventiona

266 lso sensitize tumor cells to killing via the death ligand, TRAIL.

267 nts, are sensitive to the combination of the death ligand tumor necrosis factor-related apoptosis ind

268 cinoma (CCA) cells paradoxically express the death ligand tumor necrosis factor-related apoptosis-ind

269 Recent reports have suggested that the death ligand tumor necrosis factor-related apoptosis-ind

270 cinoma (CCA) cells paradoxically express the death ligand, tumor necrosis factor-related apoptosis-in

271 expression may regulate tumor sensitivity to death ligands via inhibition of YY1 and up-regulation of

272 provide evidence that BAD may function as a death ligand whose pro-apoptotic activity requires heter

273 ivity of cancer cells to TRAIL, a TNF family death ligand with promising therapeutic potential, act b