ライフサイエンスコーパス: Fas receptor

1 fectants expressed less Fas mRNA and surface Fas receptor.

2 ns of VEGFR-2 with the cytoplasmic domain of Fas receptor.

3 uitment of both FADD and procaspase-8 to the Fas receptor.

4 verall similarity to the death domain of the Fas receptor.

5 pulation, however, showed elevated levels of Fas receptor.

6 re essential for signaling downstream of the Fas receptor.

7 n-PCR and killing of target cells expressing Fas receptor.

8 s that inhibit the apoptotic signal from the Fas receptor.

9 ation of these caspases does not involve the Fas receptor.

10 llular, versus extracellular, portion of the Fas receptor.

11 that overexpressed a truncated nonfunctional Fas receptor.

12 cascade is initiated in the cell bearing the Fas receptor.

13 ing FKBP and the intracellular domain of the Fas receptor.

14 endothelial cells to death signals from the Fas receptor.

15 induces apoptosis on cross-linking with the Fas receptor.

16 es were readily killed after ligation of the Fas receptor.

17 ible for self-association and binding to the Fas receptor.

18 amino acids of the regulatory domain of the Fas receptor.

19 nd associated with induced expression of the Fas receptor.

20 city can be inhibited by blocking Abs to the Fas receptor.

21 ose associated with apoptosis induced by the Fas receptor.

22 n to interact with the "death domain" of the Fas receptor.

23 cating a selective effect of ST6Gal-I on the Fas receptor.

24 that involves transcriptional activation of Fas receptor.

25 cell death in response to activation of the Fas receptor.

26 nding of FasL to the extracellular domain of Fas receptor.

27 a significant increase in the expression of Fas receptor.

28 n, induces apoptosis of cells expressing the Fas receptor.

29 the FKHR proteins and by stimulation of the Fas receptor.

30 e human lymphocytes by internalizing surface Fas receptors.

31 activation of the tumor necrosis factor and Fas receptors.

32 n only in target cells expressing functional Fas receptors.

33 tant process for apoptotic signaling through Fas receptors.

34 ased the glioblastoma cell death response to Fas receptor activation regardless of p53 status.

35 ppears to be, at least in part, dependent on Fas receptor activation, and plays a role in regulating

36 CF10A cells can undergo apoptosis after CD95/Fas receptor activation, cell death caused by glucocorti

37 However, in the absence of the Fas receptor, additional mechanisms of hepatocyte apopto

38 ulates endocytic compartmentalization of the Fas receptor after receptor stimulation, an important pr

39 a chains, we demonstrate that MHCII prevents Fas receptor aggregation and inhibits Fas-mediated signa

40 Treatment with Fas receptor agonists sensitized the cells to monastrol-

41 The Fas receptor (also known as CD95 and APO-1) is a member

42 l lines, CH33, sensitive to signals from the Fas receptor, although the levels of Fas were unchanged.

43 Interestingly, the upregulation of Fas receptor and expansion of SCM in acute HIV-1 infecti

44 ver, STAT-1 is critical for the induction of Fas receptor and Fas ligand expression by ischemia/reper

45 MNs in mice lacking functional Fas receptor and Fas ligand were protected from apoptosi

46 t a dose-dependent increase in the levels of Fas receptor and Fas ligand.

47 ntibodies that block the interaction between Fas receptor and FasL inhibited this cytotoxic activity.

48 This PCD pathway is triggered through the Fas receptor and involves the apoptosis signal-regulatin

49 ic mouse kidney specimens, the expression of Fas receptor and ligand proteins were markedly upregulat

50 Viral suppression reduced Fas receptor and programmed death 1 expression in lung C

51 Chicken DF-1 cells expressing human FAS receptor and susceptible to FAS-induced apoptosis we

52 SMCs stimulated with OPG is mediated via the Fas receptor and that treatment with a human antibody ta

53 dependent on the presence or absence of the Fas receptor and the duration of BDL.

54 c-receptor fusion proteins between the human Fas receptor and TNFR I, each cysteine-rich domain of Fa

55 Some changes were also found in Fas-receptor and Bak, Bax, and Bid proteins; caspase mRN

56 tients express higher membrane levels of the Fas receptor, and are particularly susceptible to apopto

57 nd (FasL) induces apoptosis of cells bearing Fas receptor, and may play a role in the acquisition of

58 egulator genes such as bcl-2 family members, Fas receptor, and other pathways.

59 xpress senescent markers, including CD57 and Fas receptor, and were moderately reduced in cell number

60 The apoptotic response was FAS receptor- and neutral sphingomyelinase-dependent and

61 caspase-9 activity, as did injection of anti-FAS-receptor antibody into either the subretinal space o

62 s were treated with a monoclonal antibody to Fas receptor (APO-1/CD95) or with various concentrations

63 Functional, soluble forms of the Fas receptor are produced by activated peripheral blood

64 h at least in part through downregulation of Fas receptor at the transcriptional level.

65 as resting NK cells become activated, their Fas receptors become competent to deliver autocrine suic

66 s was caspase dependent and occurred despite Fas receptor blockade.

67 ocked apoptosis induced by engagement of the Fas receptor but not that induced by ara-C.

68 LFG can bind to the Fas receptor, but does not regulate Fas expression or in

69 Activation of the Fas receptor by Fas-ligand (FasL) results in apoptosis,

70 this study, we show that stimulation of the Fas receptor by its ligand (FasL) induces rapid phosphor

71 Here we show that stimulation of the Fas receptor by its ligand (FasL) results in rapid gener

72 Here we show that engagement of the Fas receptor by its ligand leads to an extremely rapid a

73 nd on the FcR-stimulated NK cells with their Fas receptors can result in apoptosis of the NK cells.

74 Protein and mRNA expressions of Fas receptor, caspases-3/7/8, and Bak/Bax/Bid proteins w

75 Increased Fas-receptor (CD95) expression on CD4+ and CD8+ lymphocy

76 Ligation of the FAS-receptor (CD95) induces apoptosis by activation of p

77 Interestingly, FLAME-1 is recruited to the Fas receptor complex and can abrogate Fas/TNFR-induced a

78 These results indicate that the FasL-Fas receptor complex depends upon independent motifs loc

79 ein-mediated recruitment of caspase-8 to the Fas receptor complex in a manner that promotes caspase-8

80 n of essential ligand binding domains in the Fas receptor correlated exactly with the ability of the

81 Fas receptor cross-linking induces apoptosis in the abse

82 necessary for JNK activation in response to Fas receptor cross-linking.

83 mbrane by, for example, interaction with the Fas receptor cytoplasmic death domain (Fas-DD), or bindi

84 t with the decreased apoptosis, cell surface Fas receptor decreased significantly in tumor-induced MD

85 Similar studies were carried out in Fas receptor-defective (CBA/lpr(cg)) mice to evaluate th

86 In addition, both P-/- and Fas receptor-defective mice appeared to have a compensat

87 Similarly, Fas receptor-defective mice had a mean 3- to 3.6-fold in

88 In Fas receptor-deficient lpr mice (C57BL/6J), expression o

89 ng 2 different approaches: (1) wild-type and Fas receptor-deficient lpr mice of the C57BL/6J or C3H/H

90 Fas receptor-deficient mice had no protection against se

91 The Fas receptor delivers signals crucial for lymphocyte apo

92 Fas receptor directly binds to and activates TCR compone

93 However, the role of the Fas receptor-driven apoptotic pathway in indirect/nonpul

94 optosis induction in Jurkat T lymphocytes by Fas receptor engagement (intrinsic) or ultraviolet (UV)-

95 uman thymocytes to apoptosis induced through Fas receptor engagement, and reveal significant species-

96 significantly enhanced apoptotic response on Fas receptor engagement.

97 herapy-treated cells to agonists of the CD95/Fas receptor established that Dox and CDDP treatment sen

98 We studied the Fas receptors expressed in human thymocytes to search fo

99 us expressing Fas ligand to efficiently kill Fas receptor-expressing tumor cells.

100 sgenic mice showed a similar upregulation of Fas receptor expression and de novo expression of Fas li

101 Oncogenic ras has been shown to downregulate Fas receptor expression and increase Fas ligand expressi

102 on induced T-cell activation, apoptosis, and Fas receptor expression in humanized but not wild-type m

103 We have demonstrated that NO up-regulated Fas receptor expression in ovarian carcinoma cell lines,

104 portunistic infection had significantly more Fas receptor expression than did asymptomatic HIV-infect

105 Tumor cells strategically down-regulate Fas receptor expression to evade immune attack and up-re

106 Fas receptor expression was detected on freshly isolated

107 expression of Fas ligand and glucose-induced Fas receptor expression were observed only in 7- to 8-mo

108 the SAPK signaling pathway, by inhibition of Fas receptor expression, and by beta-adrenergic blockade

109 lso accompanied by a rapid downregulation of Fas receptor expression, non-cell cycle-related incorpor

110 ot enhance in hepatocytes that were null for FAS receptor expression.

111 l fibroblasts at both high and low levels of Fas receptor expression.

112 The reverse was true when Fas-receptor expression was evaluated.

113 inducing signalling complex (DISC) formed by Fas receptor, FADD (Fas-associated death domain protein)

114 e dehydrogenase (GAPDH)-BAX pathway; and (2) FAS receptor-FADD-caspase 8-BAX pathway.

115 (NTR), a member of the tumor necrosis factor/FAS receptor family, can modulate trk receptor function

116 f Fas ligand (FasL), while the levels of the Fas receptor (Fas) are not increased.

117 l-2-associated X protein (BAX), cell-surface Fas receptor (FAS), FASL, FAS-associated death domain, t

118 FAS receptor (FAS-R) and acidic sphingomyelinase (ASM)-d

119 FALI of the Fas receptor (Fas/CD95) using a fluorescein-conjugated a

120 Total protein levels of the Fas receptor (Fas; APO-1/CD-95) and the Fas ligand (Fas-

121 rfamily death receptor 3 (TNFRSF25, DR3) and Fas receptors (Fas) that initiate caspase cell death cas

122 Both the Fas-Receptor (Fas-R) and interleukin-1beta (IL-1beta)-co

123 ression of the apoptosis-related modulators, Fas (receptor), Fas ligand, Bax, Bcl-2, Bcl-XL, and inte

124 d in the transcriptional upregulation of the FAS-receptor, FAS-ligand, caspase-8 and BID, but not cas

125 The FAS receptor-FAS ligand system is a key apoptotic pathwa

126 gamma and tumour necrosis factor alpha, and Fas-receptor-Fas-ligand interactions.

127 istochemical methods were used to search for Fas receptor/Fas ligand system involvement in multiple s

128 The Fas-receptor/Fas-ligand (Fas-R/Fas-L) system mediates si

129 unoprecipitation was performed to assess for FAS-receptor/FAS-ligand complex formation, and activatio

130 ulted in the time-dependent formation of the FAS-receptor/FAS-ligand complex that preceded the peak o

131 combinant form of the soluble portion of the Fas receptor (FasFc).

132 The Fas ligand/Fas receptor (FasL/Fas) system is an important mediator

133 NF) family member systems, Fas ligand (FasL)-Fas receptor (FasR) and TNF-alpha-TNFR, in apoptosis of

134 en STAT3 and c-Jun results in suppression of Fas Receptor (FasR) transcription, which is often seen i

135 Jurkat) attenuated apoptosis induced by the Fas receptor (FasR).

136 Unlike soluble forms of Fas receptor, FDR dominantly inhibited apoptosis inducti

137 r correlated exactly with the ability of the Fas receptor fusion proteins to prevent cell death media

138 absence of either perforin gene function or Fas receptor gene function did not modify the course of

139 We also evaluated the Fas receptor, given its structural similarity to TNFR1.

140 e apoptosis induced through the cell-surface Fas receptor has been especially important for immunolog

141 Engagement of the Fas receptor has been reported to induce ceramide genera

142 In contrast, the corresponding region in the Fas receptor has the opposite effect and inhibits bindin

143 is by treatment with an antibody against the Fas receptor have two annexin V (AV)-binding subpopulati

144 ent stimulation of potassium channels by the Fas receptor in a human Jurkat T cell line.

145 tion of pro-apoptotic genes, NOXA, PUMA, and FAS receptor in gastric epithelial cells.

146 ecently reported increased expression of the Fas receptor in individuals with HIV infection, along wi

147 However, expression of the Fas receptor in many tumor cell types does not correlate

148 ed caspase 8 activity upon engagement of the Fas receptor in the absence of pharmacological manipulat

149 , Hip is not cleaved upon stimulation of the Fas receptor in the Jurkat T-cell line, suggesting that

150 ed reduction in cell-surface localization of Fas receptor in the transplanted cells and inhibition of

151 ransgenic animals expressing the conditional FAS receptor in thymocytes demonstrates that sensitivity

152 on of p73 activity suppressed cell death and Fas receptor induced by H pylori.

153 ggest that death receptors (DR4 and DR5) and Fas receptors induced apoptosis through identical signal

154 find that Trpm7-/- T cells are deficient in Fas-receptor-induced apoptosis and that TRPM7 channel ac

155 Fas receptor induces apoptosis of synovial bone and cart

156 Ligation of the Fas receptor induces death-inducing signaling complex (D

157 Engagement of the CD95 (APO-1/Fas) receptor induces apoptosis in a variety of cell typ

158 Thus, agonists that bind the same Fas receptor initiate mechanistically distinct pathways

159 self-association domain as well as the FIP3-Fas receptor-interacting protein interaction domain.

160 n shown to interact with various components (Fas receptor-interacting protein, NF-kappaB-inducing kin

161 The Fas receptor is a member of a family of cell death recep

162 Fas receptor is a member of the tumor necrosis factor-al

163 However, in vivo the Fas receptor is activated by its natural ligand, Fas-L,

164 The Fas receptor is composed of several discrete domains, in

165 The Fas receptor is one of a number of important physiologic

166 ily can induce cell death, e.g., the TNF and Fas receptors, it is important to determine if similar s

167 The Fas receptor ligand FasL regulates immune cell levels by

168 ocuses on the opposing functions of CD40 and Fas receptor/ligand pairs in B-cell lymphoid malignancie

169 t cells were induced to undergo apoptosis by Fas receptor ligation, cytochrome c was released from mi

170 undergo the normal degree of apoptosis after Fas receptor ligation.

171 ible for activating a protease cascade after Fas-receptor ligation, leading to cell death.

172 letion and markedly reduced the incidence of Fas-receptor localization in GM1 rafts.

173 a type 2 cytokine response attributable to a Fas-receptor mediated clearance of antigen-specific IFN-

174 effector caspases and apoptotic nucleases in Fas receptor-mediated apoptosis of Jurkat cells, althoug

175 n species production and cell death, but not FAS receptor-mediated apoptosis.

176 irmed that Lupeol specifically activates the Fas receptor-mediated apoptotic pathway in androgen-sens

177 eviously unidentified model of resistance to Fas receptor-mediated liver failure in the wild-derived

178 The Fas receptor mediates a signalling cascade resulting in

179 Increased Fas receptor membrane targeting suggests that apoptosis

180 In isolated macrophages, stimulation of Fas receptor minimally enhances lipopolysaccharide-induc

181 revealed increased levels of nuclear p53 and Fas receptor mRNA but without corresponding increases in

182 MRL-lpr/lpr mice have a Fas receptor mutation that leads to abnormalities of apo

183 When studies were performed in Fas receptor-negative C3H.(lpr) mice, the adverse effect

184 osis and necrosis, including blockage of the Fas receptor, neuroprotective peptides and antioxidants,

185 Heterozygous mutations in the CD95 (APO-1/Fas) receptor occur in most individuals with autoimmune

186 e that NO up-regulates the expression of the Fas receptor on AD10 cells via the specific inactivation

187 of a small peptide inhibitor (Met12) of the Fas receptor on the activation of extrinsic and intrinsi

188 Expression of the Fas receptor on the B lymphoma cell lines did not correl

189 The expression of Fas receptor on three gastric epithelial cell lines was

190 of Met12, a small molecule inhibitor of the Fas receptor, on LC3-I to LC3-II conversion and Atg5 exp

191 Caspase 8 is immediately recruited to the Fas receptor once it oligomerizes, and its protease acti

192 by an immunoglobulin M antibody against the fas receptor or by tumor necrosis factor alpha.

193 Mutations in the Fas receptor or its ligand (FasL) lead to lupus-like sys

194 NA damaging agents up-regulate levels of the Fas receptor or its ligand, resulting in recruitment of

195 was not due to lack of expression of either Fas receptor or its ligand.

196 Genetic abnormalities in the Fas receptor or its trimeric ligand, FasL, result in mas

197 erexpression of full length or bioengineered Fas receptors or were transduced with a retroviral Fas e

198 r neutralizing antibodies against either the FAS-receptor or FAS-ligand.

199 ptors, such as the tumor necrosis factor and Fas receptors, PAK4 can inhibit the death signal by a di

200 omide efficacy by blunting activation of the Fas receptor pathway in p53(+/+) glioma cells.

201 iral factors and can act in synergy with the Fas receptor pathway, thereby enhancing the apoptotic pr

202 t may regulate apoptosis induced by the CD95/Fas receptor pathway.

203 pendent apoptosis via both mitochondrial and Fas receptor pathways, which were abrogated in the prese

204 onstrated that interferon gamma, but not the Fas receptor, played a critical role in the suppression.

205 Signal transduction through the Fas receptor plays no essential role in the induction of

206 tion of caspase-8, as well as an increase in Fas receptor polarization.

207 se defects are accompanied by impairments in Fas receptor polarization.

208 immune cell levels by inducing apoptosis of Fas receptor-positive cells.

209 and induces apoptosis in tumor-infiltrating, Fas receptor-positive lymphocytes.

210 report we demonstrate that activation of the Fas receptor present on a human breast epithelial cell l

211 The Fas receptor rapidly induces apoptosis when activated by

212 r necrosis factor receptor 1 (TNFR1) and the Fas receptor recruit complexes formed by the interaction

213 In controls, activation of the Fas receptor resulted in rapid dephosphorylation of Bid

214 Basolateral cross-linking of the Fas receptor resulted in T84 cell apoptosis and a loss o

215 Ligation of the Fas receptor resulted in the rapid stimulation of ICE pr

216 s cell cycling and induces expression of the Fas-receptor, resulting in subsequent apoptosis of hemat

217 es of key apoptosis mediators downstream the Fas receptor revealed that expression levels of IRF8 and

218 ssary component of JNK activation induced by Fas receptor signaling and that PAK2 can contribute to t

219 Although current approaches prevent Fas receptor signaling by excluding FasL binding to Fas,

220 Apoptosis mediated by Fas receptor signaling is not the mechanism of clonal de

221 Here, we show that Fas receptor signaling requires a functional T-cell rece

222 corticoid withdrawal is independent of CD95/ Fas receptor signaling.

223 This is demonstrated by evolution of an anti-Fas receptor single-chain variable fragment (scFv) that

224 The Fas receptor stimulates apoptosis, and artificial dimeri

225 rs of this response and tested the effect of Fas receptor-stimulating antibody on corneal stromal fib

226 Fas receptor stimulation does not activate canonical dow

227 vation of Lck and downstream signaling after Fas receptor stimulation.

228 n response to tumor necrosis factor alpha or Fas-receptor stimulation.

229 in vivo, we used conditional alleles of the Fas receptor that can be triggered by an intracellularly

230 scribe here a unique, membrane-bound form of Fas receptor that contained a complete extracellular dom

231 ot with other TNF family members such as the Fas receptor, the p75 TNF receptor, and p75 neurotrophin

232 ependent interaction of wild-type and mutant Fas receptors through a specific region in the extracell

233 naling pathways leading from ligation of the Fas receptor to induction of apoptosis.

234 In cultured podocytes, cross-linking of the Fas receptor to mimic ligand binding induced caspase 8 a

235 causing ligand independent activation of the FAS receptor to stimulate an apoptotic response, which i

236 that receives the activation signal from the Fas-receptor to initiate the apoptotic protease cascade

237 ne Fas (also known as Tnfrsf6), encoding the Fas receptor, to protect mice from liver failure and fib

238 significantly decreased in most cases after Fas receptor triggering and increased by Fas ligand (Fas

239 nctions of Fas, it was not clear whether the Fas receptor was an essential mediator of beta cell deat

240 ar levels of the TNF-receptor I, whereas the Fas receptor was detected only in HL-525 cells.

241 nt clones were susceptible to apoptosis when Fas receptor was directly ligated by anti-Fas antibodies

242 death domain (FADD) and procaspase-8 to the Fas receptor was examined via analysis of death-inducing

243 In addition, Fas receptor was induced, but to a lesser extent, in num

244 The Fas receptor was strongly expressed in hepatocytes in li

245 In addition, Fas receptor was up-regulated in A549 cells in response

246 imeric receptors of p75(NTR) and the related Fas receptor, we have identified domains that are essent

247 spread induction of PCD, transcripts for the Fas receptor were detected in all chambers of the heart

248 Agonistic antibodies against the Fas receptor, when administered to mice in vivo, cause s

249 d reactivated expression of the proapoptotic Fas receptor, which is also down-regulated by Ras.

250 cells Bid was cleaved upon activation of the Fas receptor with an anti-Fas antibody.

251 exchanging different domains of noncleavable Fas receptor with p75(NTR), however, revealed that a dis

252 Ligation of Fas receptor with recombinant sFasL triggered apoptosis

253 e autoimmune syndrome due to a dysfunctional Fas receptor, with contributions from other less well-de