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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 n-PCR and killing of target cells expressing Fas receptor.
7 s that inhibit the apoptotic signal from the Fas receptor.
8 ation of these caspases does not involve the Fas receptor.
9 llular, versus extracellular, portion of the Fas receptor.
10 that overexpressed a truncated nonfunctional Fas receptor.
11 cascade is initiated in the cell bearing the Fas receptor.
12 ing FKBP and the intracellular domain of the Fas receptor.
13  endothelial cells to death signals from the Fas receptor.
14  induces apoptosis on cross-linking with the Fas receptor.
15 es were readily killed after ligation of the Fas receptor.
16 ible for self-association and binding to the Fas receptor.
17  amino acids of the regulatory domain of the Fas receptor.
18 nd associated with induced expression of the Fas receptor.
19 city can be inhibited by blocking Abs to the Fas receptor.
20 cating a selective effect of ST6Gal-I on 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  that involves transcriptional activation of Fas receptor.
24  cell death in response to activation of the Fas receptor.
25  a significant increase in the expression of Fas receptor.
26 n, induces apoptosis of cells expressing the Fas receptor.
27 re essential for signaling downstream of the Fas receptor.
28  the FKHR proteins and by stimulation of the Fas receptor.
29  activation of the tumor necrosis factor and Fas receptors.
30 tant process for apoptotic signaling through Fas receptors.
31 n only in target cells expressing functional Fas receptors.
32 e human lymphocytes by internalizing surface Fas receptors.
33 ased the glioblastoma cell death response to Fas receptor activation regardless of p53 status.
34 ppears to be, at least in part, dependent on Fas receptor activation, and plays a role in regulating
35 CF10A cells can undergo apoptosis after CD95/Fas receptor activation, cell death caused by glucocorti
36               However, in the absence of the Fas receptor, additional mechanisms of hepatocyte apopto
37 ulates endocytic compartmentalization of the Fas receptor after receptor stimulation, an important pr
38 a chains, we demonstrate that MHCII prevents Fas receptor aggregation and inhibits Fas-mediated signa
39                               Treatment with Fas receptor agonists sensitized the cells to monastrol-
40                                          The Fas receptor (also known as CD95 and APO-1) is a member
41 l lines, CH33, sensitive to signals from the Fas receptor, although the levels of Fas were unchanged.
42 ver, STAT-1 is critical for the induction of Fas receptor and Fas ligand expression by ischemia/reper
43               MNs in mice lacking functional Fas receptor and Fas ligand were protected from apoptosi
44 t a dose-dependent increase in the levels of Fas receptor and Fas ligand.
45 ntibodies that block the interaction between Fas receptor and FasL inhibited this cytotoxic activity.
46    This PCD pathway is triggered through the Fas receptor and involves the apoptosis signal-regulatin
47 ic mouse kidney specimens, the expression of Fas receptor and ligand proteins were markedly upregulat
48                    Viral suppression reduced Fas receptor and programmed death 1 expression in lung C
49          Chicken DF-1 cells expressing human FAS receptor and susceptible to FAS-induced apoptosis we
50  dependent on the presence or absence of the Fas receptor and the duration of BDL.
51 c-receptor fusion proteins between the human Fas receptor and TNFR I, each cysteine-rich domain of Fa
52              Some changes were also found in Fas-receptor and Bak, Bax, and Bid proteins; caspase mRN
53 tients express higher membrane levels of the Fas receptor, and are particularly susceptible to apopto
54 nd (FasL) induces apoptosis of cells bearing Fas receptor, and may play a role in the acquisition of
55 egulator genes such as bcl-2 family members, Fas receptor, and other pathways.
56 xpress senescent markers, including CD57 and Fas receptor, and were moderately reduced in cell number
57                   The apoptotic response was FAS receptor- and neutral sphingomyelinase-dependent and
58 caspase-9 activity, as did injection of anti-FAS-receptor antibody into either the subretinal space o
59 s were treated with a monoclonal antibody to Fas receptor (APO-1/CD95) or with various concentrations
60             Functional, soluble forms of the Fas receptor are produced by activated peripheral blood
61 h at least in part through downregulation of Fas receptor at the transcriptional level.
62  as resting NK cells become activated, their Fas receptors become competent to deliver autocrine suic
63 s was caspase dependent and occurred despite Fas receptor blockade.
64 ocked apoptosis induced by engagement of the Fas receptor but not that induced by ara-C.
65                          LFG can bind to the Fas receptor, but does not regulate Fas expression or in
66                            Activation of the Fas receptor by Fas-ligand (FasL) results in apoptosis,
67  this study, we show that stimulation of the Fas receptor by its ligand (FasL) induces rapid phosphor
68         Here we show that stimulation of the Fas receptor by its ligand (FasL) results in rapid gener
69          Here we show that engagement of the Fas receptor by its ligand leads to an extremely rapid a
70 nd on the FcR-stimulated NK cells with their Fas receptors can result in apoptosis of the NK cells.
71              Protein and mRNA expressions of Fas receptor, caspases-3/7/8, and Bak/Bax/Bid proteins w
72                                    Increased Fas-receptor (CD95) expression on CD4+ and CD8+ lymphocy
73                              Ligation of the FAS-receptor (CD95) induces apoptosis by activation of p
74   Interestingly, FLAME-1 is recruited to the Fas receptor complex and can abrogate Fas/TNFR-induced a
75         These results indicate that the FasL-Fas receptor complex depends upon independent motifs loc
76 ein-mediated recruitment of caspase-8 to the Fas receptor complex in a manner that promotes caspase-8
77 n of essential ligand binding domains in the Fas receptor correlated exactly with the ability of the
78                                              Fas receptor cross-linking induces apoptosis in the abse
79  necessary for JNK activation in response to Fas receptor cross-linking.
80 mbrane by, for example, interaction with the Fas receptor cytoplasmic death domain (Fas-DD), or bindi
81 t with the decreased apoptosis, cell surface Fas receptor decreased significantly in tumor-induced MD
82          Similar studies were carried out in Fas receptor-defective (CBA/lpr(cg)) mice to evaluate th
83                   In addition, both P-/- and Fas receptor-defective mice appeared to have a compensat
84                                   Similarly, Fas receptor-defective mice had a mean 3- to 3.6-fold in
85                                           In Fas receptor-deficient lpr mice (C57BL/6J), expression o
86 ng 2 different approaches: (1) wild-type and Fas receptor-deficient lpr mice of the C57BL/6J or C3H/H
87                                              Fas receptor-deficient mice had no protection against se
88                                          The Fas receptor delivers signals crucial for lymphocyte apo
89                                              Fas receptor directly binds to and activates TCR compone
90                     However, the role of the Fas receptor-driven apoptotic pathway in indirect/nonpul
91 optosis induction in Jurkat T lymphocytes by Fas receptor engagement (intrinsic) or ultraviolet (UV)-
92 uman thymocytes to apoptosis induced through Fas receptor engagement, and reveal significant species-
93 significantly enhanced apoptotic response on Fas receptor engagement.
94 herapy-treated cells to agonists of the CD95/Fas receptor established that Dox and CDDP treatment sen
95                               We studied the Fas receptors expressed in human thymocytes to search fo
96 us expressing Fas ligand to efficiently kill Fas receptor-expressing tumor cells.
97 sgenic mice showed a similar upregulation of Fas receptor expression and de novo expression of Fas li
98 Oncogenic ras has been shown to downregulate Fas receptor expression and increase Fas ligand expressi
99 on induced T-cell activation, apoptosis, and Fas receptor expression in humanized but not wild-type m
100    We have demonstrated that NO up-regulated Fas receptor expression in ovarian carcinoma cell lines,
101 portunistic infection had significantly more Fas receptor expression than did asymptomatic HIV-infect
102      Tumor cells strategically down-regulate Fas receptor expression to evade immune attack and up-re
103                                              Fas receptor expression was detected on freshly isolated
104 expression of Fas ligand and glucose-induced Fas receptor expression were observed only in 7- to 8-mo
105 the SAPK signaling pathway, by inhibition of Fas receptor expression, and by beta-adrenergic blockade
106 lso accompanied by a rapid downregulation of Fas receptor expression, non-cell cycle-related incorpor
107 ot enhance in hepatocytes that were null for FAS receptor expression.
108 l fibroblasts at both high and low levels of Fas receptor expression.
109                    The reverse was true when Fas-receptor expression was evaluated.
110 inducing signalling complex (DISC) formed by Fas receptor, FADD (Fas-associated death domain protein)
111 e dehydrogenase (GAPDH)-BAX pathway; and (2) FAS receptor-FADD-caspase 8-BAX pathway.
112 (NTR), a member of the tumor necrosis factor/FAS receptor family, can modulate trk receptor function
113 f Fas ligand (FasL), while the levels of the Fas receptor (Fas) are not increased.
114 l-2-associated X protein (BAX), cell-surface Fas receptor (FAS), FASL, FAS-associated death domain, t
115                                              FAS receptor (FAS-R) and acidic sphingomyelinase (ASM)-d
116                                  FALI of the Fas receptor (Fas/CD95) using a fluorescein-conjugated a
117                  Total protein levels of the Fas receptor (Fas; APO-1/CD-95) and the Fas ligand (Fas-
118                                     Both the Fas-Receptor (Fas-R) and interleukin-1beta (IL-1beta)-co
119 ression of the apoptosis-related modulators, Fas (receptor), Fas ligand, Bax, Bcl-2, Bcl-XL, and inte
120 d in the transcriptional upregulation of the FAS-receptor, FAS-ligand, caspase-8 and BID, but not cas
121                                          The FAS receptor-FAS ligand system is a key apoptotic pathwa
122 istochemical methods were used to search for Fas receptor/Fas ligand system involvement in multiple s
123                                          The Fas-receptor/Fas-ligand (Fas-R/Fas-L) system mediates si
124 unoprecipitation was performed to assess for FAS-receptor/FAS-ligand complex formation, and activatio
125 ulted in the time-dependent formation of the FAS-receptor/FAS-ligand complex that preceded the peak o
126 combinant form of the soluble portion of the Fas receptor (FasFc).
127                               The Fas ligand/Fas receptor (FasL/Fas) system is an important mediator
128 NF) family member systems, Fas ligand (FasL)-Fas receptor (FasR) and TNF-alpha-TNFR, in apoptosis of
129 en STAT3 and c-Jun results in suppression of Fas Receptor (FasR) transcription, which is often seen i
130                      Unlike soluble forms of Fas receptor, FDR dominantly inhibited apoptosis inducti
131 r correlated exactly with the ability of the Fas receptor fusion proteins to prevent cell death media
132  absence of either perforin gene function or Fas receptor gene function did not modify the course of
133 e apoptosis induced through the cell-surface Fas receptor has been especially important for immunolog
134                            Engagement of the Fas receptor has been reported to induce ceramide genera
135 In contrast, the corresponding region in the Fas receptor has the opposite effect and inhibits bindin
136 is by treatment with an antibody against the Fas receptor have two annexin V (AV)-binding subpopulati
137 ent stimulation of potassium channels by the Fas receptor in a human Jurkat T cell line.
138 tion of pro-apoptotic genes, NOXA, PUMA, and FAS receptor in gastric epithelial cells.
139 ecently reported increased expression of the Fas receptor in individuals with HIV infection, along wi
140                   However, expression of the Fas receptor in many tumor cell types does not correlate
141 ed caspase 8 activity upon engagement of the Fas receptor in the absence of pharmacological manipulat
142 , Hip is not cleaved upon stimulation of the Fas receptor in the Jurkat T-cell line, suggesting that
143 ed reduction in cell-surface localization of Fas receptor in the transplanted cells and inhibition of
144 ransgenic animals expressing the conditional FAS receptor in thymocytes demonstrates that sensitivity
145 on of p73 activity suppressed cell death and Fas receptor induced by H pylori.
146 ggest that death receptors (DR4 and DR5) and Fas receptors induced apoptosis through identical signal
147  find that Trpm7-/- T cells are deficient in Fas-receptor-induced apoptosis and that TRPM7 channel ac
148                              Ligation of the Fas receptor induces death-inducing signaling complex (D
149                Engagement of the CD95 (APO-1/Fas) receptor induces apoptosis in a variety of cell typ
150            Thus, agonists that bind the same Fas receptor initiate mechanistically distinct pathways
151  self-association domain as well as the FIP3-Fas receptor-interacting protein interaction domain.
152 n shown to interact with various components (Fas receptor-interacting protein, NF-kappaB-inducing kin
153                                          The Fas receptor is a member of a family of cell death recep
154                                              Fas receptor is a member of the tumor necrosis factor-al
155                         However, in vivo the Fas receptor is activated by its natural ligand, Fas-L,
156                                          The Fas receptor is composed of several discrete domains, in
157                                          The Fas receptor is one of a number of important physiologic
158 ily can induce cell death, e.g., the TNF and Fas receptors, it is important to determine if similar s
159                                          The Fas receptor ligand FasL regulates immune cell levels by
160 ocuses on the opposing functions of CD40 and Fas receptor/ligand pairs in B-cell lymphoid malignancie
161 t cells were induced to undergo apoptosis by Fas receptor ligation, cytochrome c was released from mi
162 undergo the normal degree of apoptosis after Fas receptor ligation.
163 ible for activating a protease cascade after Fas-receptor ligation, leading to cell death.
164 letion and markedly reduced the incidence of Fas-receptor localization in GM1 rafts.
165 a type 2 cytokine response attributable to a Fas-receptor mediated clearance of antigen-specific IFN-
166 effector caspases and apoptotic nucleases in Fas receptor-mediated apoptosis of Jurkat cells, althoug
167 irmed that Lupeol specifically activates the Fas receptor-mediated apoptotic pathway in androgen-sens
168 eviously unidentified model of resistance to Fas receptor-mediated liver failure in the wild-derived
169                                          The Fas receptor mediates a signalling cascade resulting in
170                                    Increased Fas receptor membrane targeting suggests that apoptosis
171      In isolated macrophages, stimulation of Fas receptor minimally enhances lipopolysaccharide-induc
172 revealed increased levels of nuclear p53 and Fas receptor mRNA but without corresponding increases in
173                      MRL-lpr/lpr mice have a Fas receptor mutation that leads to abnormalities of apo
174               When studies were performed in Fas receptor-negative C3H.(lpr) mice, the adverse effect
175 osis and necrosis, including blockage of the Fas receptor, neuroprotective peptides and antioxidants,
176    Heterozygous mutations in the CD95 (APO-1/Fas) receptor occur in most individuals with autoimmune
177 e that NO up-regulates the expression of the Fas receptor on AD10 cells via the specific inactivation
178  of a small peptide inhibitor (Met12) of the Fas receptor on the activation of extrinsic and intrinsi
179                            Expression of the Fas receptor on the B lymphoma cell lines did not correl
180                            The expression of Fas receptor on three gastric epithelial cell lines was
181  of Met12, a small molecule inhibitor of the Fas receptor, on LC3-I to LC3-II conversion and Atg5 exp
182    Caspase 8 is immediately recruited to the Fas receptor once it oligomerizes, and its protease acti
183  by an immunoglobulin M antibody against the fas receptor or by tumor necrosis factor alpha.
184                             Mutations in the Fas receptor or its ligand (FasL) lead to lupus-like sys
185 NA damaging agents up-regulate levels of the Fas receptor or its ligand, resulting in recruitment of
186  was not due to lack of expression of either Fas receptor or its ligand.
187                 Genetic abnormalities in the Fas receptor or its trimeric ligand, FasL, result in mas
188 erexpression of full length or bioengineered Fas receptors or were transduced with a retroviral Fas e
189 r neutralizing antibodies against either the FAS-receptor or FAS-ligand.
190 ptors, such as the tumor necrosis factor and Fas receptors, PAK4 can inhibit the death signal by a di
191 omide efficacy by blunting activation of the Fas receptor pathway in p53(+/+) glioma cells.
192 iral factors and can act in synergy with the Fas receptor pathway, thereby enhancing the apoptotic pr
193 t may regulate apoptosis induced by the CD95/Fas receptor pathway.
194 pendent apoptosis via both mitochondrial and Fas receptor pathways, which were abrogated in the prese
195 onstrated that interferon gamma, but not the Fas receptor, played a critical role in the suppression.
196              Signal transduction through the Fas receptor plays no essential role in the induction of
197 tion of caspase-8, as well as an increase in Fas receptor polarization.
198 se defects are accompanied by impairments in Fas receptor polarization.
199  immune cell levels by inducing apoptosis of Fas receptor-positive cells.
200 report we demonstrate that activation of the Fas receptor present on a human breast epithelial cell l
201                                          The Fas receptor rapidly induces apoptosis when activated by
202 r necrosis factor receptor 1 (TNFR1) and the Fas receptor recruit complexes formed by the interaction
203               In controls, activation of the Fas receptor resulted in rapid dephosphorylation of Bid
204             Basolateral cross-linking of the Fas receptor resulted in T84 cell apoptosis and a loss o
205                              Ligation of the Fas receptor resulted in the rapid stimulation of ICE pr
206 s cell cycling and induces expression of the Fas-receptor, resulting in subsequent apoptosis of hemat
207 es of key apoptosis mediators downstream the Fas receptor revealed that expression levels of IRF8 and
208 ssary component of JNK activation induced by Fas receptor signaling and that PAK2 can contribute to t
209          Although current approaches prevent Fas receptor signaling by excluding FasL binding to Fas,
210                        Apoptosis mediated by Fas receptor signaling is not the mechanism of clonal de
211                           Here, we show that Fas receptor signaling requires a functional T-cell rece
212 corticoid withdrawal is independent of CD95/ Fas receptor signaling.
213 This is demonstrated by evolution of an anti-Fas receptor single-chain variable fragment (scFv) that
214                                          The Fas receptor stimulates apoptosis, and artificial dimeri
215 rs of this response and tested the effect of Fas receptor-stimulating antibody on corneal stromal fib
216                                              Fas receptor stimulation does not activate canonical dow
217 vation of Lck and downstream signaling after Fas receptor stimulation.
218 n response to tumor necrosis factor alpha or Fas-receptor stimulation.
219  in vivo, we used conditional alleles of the Fas receptor that can be triggered by an intracellularly
220 scribe here a unique, membrane-bound form of Fas receptor that contained a complete extracellular dom
221 ot with other TNF family members such as the Fas receptor, the p75 TNF receptor, and p75 neurotrophin
222 ependent interaction of wild-type and mutant Fas receptors through a specific region in the extracell
223 naling pathways leading from ligation of the Fas receptor to induction of apoptosis.
224  In cultured podocytes, cross-linking of the Fas receptor to mimic ligand binding induced caspase 8 a
225 causing ligand independent activation of the FAS receptor to stimulate an apoptotic response, which i
226 that receives the activation signal from the Fas-receptor to initiate the apoptotic protease cascade
227 ne Fas (also known as Tnfrsf6), encoding the Fas receptor, to protect mice from liver failure and fib
228  significantly decreased in most cases after Fas receptor triggering and increased by Fas ligand (Fas
229 nctions of Fas, it was not clear whether the Fas receptor was an essential mediator of beta cell deat
230 ar levels of the TNF-receptor I, whereas the Fas receptor was detected only in HL-525 cells.
231 nt clones were susceptible to apoptosis when Fas receptor was directly ligated by anti-Fas antibodies
232  death domain (FADD) and procaspase-8 to the Fas receptor was examined via analysis of death-inducing
233                                 In addition, Fas receptor was induced, but to a lesser extent, in num
234                                          The Fas receptor was strongly expressed in hepatocytes in li
235                                 In addition, Fas receptor was up-regulated in A549 cells in response
236 imeric receptors of p75(NTR) and the related Fas receptor, we have identified domains that are essent
237 spread induction of PCD, transcripts for the Fas receptor were detected in all chambers of the heart
238             Agonistic antibodies against the Fas receptor, when administered to mice in vivo, cause s
239 d reactivated expression of the proapoptotic Fas receptor, which is also down-regulated by Ras.
240 cells Bid was cleaved upon activation of the Fas receptor with an anti-Fas antibody.
241 exchanging different domains of noncleavable Fas receptor with p75(NTR), however, revealed that a dis
242                                  Ligation of Fas receptor with recombinant sFasL triggered apoptosis
243 e autoimmune syndrome due to a dysfunctional Fas receptor, with contributions from other less well-de

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