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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.
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
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
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
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
51 c-receptor fusion proteins between the human Fas receptor and TNFR I, each cysteine-rich domain of Fa
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
56 xpress senescent markers, including CD57 and Fas receptor, and were moderately reduced in cell number
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
62 as resting NK cells become activated, their Fas receptors become competent to deliver autocrine suic
67 this study, we show that stimulation of the Fas receptor by its ligand (FasL) induces rapid phosphor
70 nd on the FcR-stimulated NK cells with their Fas receptors can result in apoptosis of the NK cells.
74 Interestingly, FLAME-1 is recruited to the Fas receptor complex and can abrogate Fas/TNFR-induced a
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
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
86 ng 2 different approaches: (1) wild-type and Fas receptor-deficient lpr mice of the C57BL/6J or C3H/H
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-
94 herapy-treated cells to agonists of the CD95/Fas receptor established that Dox and CDDP treatment sen
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
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
110 inducing signalling complex (DISC) formed by Fas receptor, FADD (Fas-associated death domain protein)
112 (NTR), a member of the tumor necrosis factor/FAS receptor family, can modulate trk receptor function
114 l-2-associated X protein (BAX), cell-surface Fas receptor (FAS), FASL, FAS-associated death domain, t
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
122 istochemical methods were used to search for Fas receptor/Fas ligand system involvement in multiple s
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
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
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
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
139 ecently reported increased expression of the Fas receptor in individuals with HIV infection, along wi
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
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
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
158 ily can induce cell death, e.g., the TNF and Fas receptors, it is important to determine if similar s
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
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
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
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
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
185 NA damaging agents up-regulate levels of the Fas receptor or its ligand, resulting in recruitment of
188 erexpression of full length or bioengineered Fas receptors or were transduced with a retroviral Fas e
190 ptors, such as the tumor necrosis factor and Fas receptors, PAK4 can inhibit the death signal by a di
192 iral factors and can act in synergy with the Fas receptor pathway, thereby enhancing the apoptotic pr
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.
200 report we demonstrate that activation of the Fas receptor present on a human breast epithelial cell l
202 r necrosis factor receptor 1 (TNFR1) and the Fas receptor recruit complexes formed by the interaction
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
213 This is demonstrated by evolution of an anti-Fas receptor single-chain variable fragment (scFv) that
215 rs of this response and tested the effect of Fas receptor-stimulating antibody on corneal stromal fib
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
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
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
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
241 exchanging different domains of noncleavable Fas receptor with p75(NTR), however, revealed that a dis
243 e autoimmune syndrome due to a dysfunctional Fas receptor, with contributions from other less well-de
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