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(Received for publication, December 1, 1995) From the
CD95 (Fas/APO-1) and tumor necrosis factor receptor-1 (TNFR-1)
are related molecules that signal apoptosis. Recently, a number of
novel binding proteins have been proposed to mediate the signaling of
these death receptors. Here we report that an N-terminal truncation of
one of these candidate signal transducers, FADD/MORT1, abrogates
CD95-induced apoptosis, ceramide generation, and activation of the cell
death protease Yama/CPP32. In addition, this dominant-negative
derivative of FADD (FADD-DN) blocked TNF-induced apoptosis while not
affecting NF-
Recently, major advances have been made in understanding the
signal transduction of the tumor necrosis factor
(TNF)(
Overexpression of FADD causes apoptosis(9) ,
resulting in cleavage of the death substrate poly(ADP-ribose)
polymerase (PARP) to signature apoptotic fragments (data not shown). A
previously reported deletion mutant of FADD, NFD4 (hereon referred to
as FADD-DN), was able to interact with CD95, but failed to initiate
apoptosis (9) (Fig. 1A), suggesting that it may
have a dominant negative effect on CD95 signaling. FADD-DN lacks 80
N-terminal amino acids, but contains the death domain responsible for
association with the related death domain of CD95(9) . The B
lymphoma cell line BJAB was transfected with either the expression
vector pcDNA3 alone or as a FADD-DN expression construct. Stable
transfectants were generated by neomycin (G418) selection and pooled
populations assessed for FADD-DN expression and sensitivity to
anti-Fas-induced apoptosis (BJAB-FADD-DN, Fig. 1B).
Expression of FADD-DN in both a pooled population and in a mixture of
selected clones (BJAB-sFADD-DN) dramatically abrogated
CD95-induced cell death (Fig. 1B). The apoptotic nature
of the cell death was confirmed by the TUNEL assay which detects 3`-OH
DNA strand breaks. The FADD-DN expressing BJAB cells were not
inherently resistant to apoptotic cell death, since the protein kinase
inhibitor staurosporine and the calcium ionophore A23187 equally killed
the three cell lines (data not shown). CD95 surface expression was
equivalent in the vector and FADD-DN cell lines as assessed by flow
cytometry (data not shown). The possibility that clonal variation in
the stable lines was responsible for the observed resistance to CD95
killing was discounted by the observation that transient overexpression
of the FADD derivative ablated CD95-induced cell death in BJAB and
Jurkat cells (data not shown).
Figure 1:
FADD
mediates CD95 signal transduction. A, schematic representation
of FADD and FADD-DN (NFD-4). Amino acid residues are given for
selected junctures. B, BJAB cells expressing FADD-DN are
resistant to CD95-induced apoptosis. The indicated cell lines were
incubated for 16 h with various concentrations of anti-Fas IgM and cell
death assessed by nuclear morphology. At least 250 cells were counted
in three independent experiments (mean ± S.D.). Expression of
FADD-DN is shown in the photographic insets. FADD-DN migrates
as a doublet around 18 kDa due to post-translational modification(23).
The TUNEL assay is shown in the graphical inset, and at least
250 cells were counted in three independent experiments (mean ±
S.D.). C, anti-CD95-induced ceramide generation is abrogated
by FADD-DN. The indicated BJAB cell lines were treated with anti-Fas
IgM (1 µg/ml) for the various times listed and ceramide levels
subsequently assessed (mean ± S.D.; n = 3).
Significant levels of ceramide could not be detected at 5-, 10-, 30-
and 60-min time points (inset). D,
C
The sphingolipid ceramide has been
implicated as a signaling intermediate in the CD95
pathway(20, 24, 25, 26) . To
determine whether this signaling event was blocked by the FADD
derivative, BJAB cells expressing FADD-DN were treated with anti-Fas
IgM and, subsequently, ceramide levels assessed. Consistent with a
proximal role of FADD in CD95 signaling, FADD-DN inhibited
CD95-mediated ceramide generation (Fig. 1C).
Additionally, vector and FADD-DN transfected BJAB cells were equally
susceptible to cell death induced by the cell-permeable, active
ceramide analogue, C Mammalian homologs of the Caenorhabditis elegans cell death protease CED-3 are thought
to be distal effectors of the CD95 cell death pathway. Here we show
that the apoptotic protease Yama/CPP32 (17, 27, 28) is activated by CD95 engagement (Fig. 1E). Endogenous Yama is expressed as a 32-kDa
pro-enzyme and upon activation is proteolytically processed into active
p17 and p12 subunits(17, 27) . One of the proposed
substrates of Yama is the nuclear enzyme
PARP(17, 27) . As expected, CD95-mediated activation
of Yama and resulting PARP cleavage was blocked by FADD-DN (Fig. 1E). In the yeast two-hybrid assay, FADD had a
weak but specific interaction with TNFR-1(9) . To determine
whether FADD has a role in TNFR-1-induced cell death, the FADD
derivative was transfected into TNF-sensitive MCF7 breast carcinoma
cells and stable cell lines generated. Interestingly, FADD-DN
expressing MCF7 cells were equally resistant to both CD95- and
TNF-induced cell death (Fig. 2A, Table 1),
suggesting a proximal convergence of the cytokine-mediated cell death
pathway. Additionally, 293T cells transiently overexpressing TNFR-1
were protected from cell death by co-transfecting FADD-DN (data not
shown). As with the BJAB cell lines, the FADD-DN MCF7 cell lines were
not resistant to staurosporine-induced apoptosis (Table 1).
Overexpression of interleukin-1
Figure 2:
FADD mediates TNF-induced cell death, but
not TNF-induced NF-
While the main activity of CD95 is to trigger apoptosis, TNFR-1 can
signal an array of diverse pro-inflammatory and immunoregulatory
activities(29) . Distinct from CD95, TNFR-1 is an inducer of
nuclear factor To determine the mechanism by
which the FADD derivative exerts its dominant negative effect,
co-immunoprecipitation of FADD and FADD-DN with CD95 or TNFR-1 was
assessed. 293T cells were co-transfected with AU1 epitope-tagged FADD
constructs and FLAG epitope-tagged CD95, FLAG-TNFR-1, or
FLAG-B94(31) . Cell lysates were immunoprecipitated with
anti-FADD antibody and subsequently immunoblotted with anti-FLAG
antibody. TNFR-1 and CD95, but not a control cytoplasmic protein, B94,
co-immunoprecipitated with FADD-DN (Fig. 3A). The
association of FADD and FADD-DN with CD95 was 10-fold greater than with
TNFR-1, correlating with the relative apoptotic potential of the two
death receptors(32) . Thus, our data suggest that FADD-DN
exerts its inhibitory action by directly or indirectly forming a
complex with the death receptors, preventing recruitment of endogenous
FADD. It remains formally possible, however, that FADD-DN functions by
binding and sequestering other death signaling molecules.
Figure 3:
A mechanism for the inhibitory action of
FADD-DN. A, 293T cells were co-transfected with AU1 epitope
tagged FADD constructs and FLAG-tagged constructs encoding CD95,
TNFR-1, and B94. The cells were lysed and FADD, or FADD-DN was
immunoprecipitated with anti-FADD polyclonal antibody, run on a 15%
SDS-polyacrylamide gel, and subsequently transferred to a
nitrocellulose membrane. Co-precipitating FLAG-Fas and FLAG-TNFR-1 were
identified by immunoblotting with anti-FLAG antibody. B94, a 73-kDa
protein(31) , did not co-precipitate with FADD, verifying the
specificity of the protein-protein interaction. All transfected
components were assessed for expression by immunoblotting cell lysates
(data not shown). B, a truncated derivative of FADD exerts a
dominant-negative effect by displacing endogenous FADD from activated
CD95 and thereby inhibits DISC formation. BJAB vector (upper
panels) and BJAB-sFADD-DN cells (middle panels) were
metabolically labeled (with [
In the
case of CD95, the endogenous signaling machinery was studied. Four
proteins, termed CAPs (for cytotoxicity-dependent APO-1-associated
proteins), associate with CD95 in a ligand-dependent
fashion(23) . CAP1 and CAP2 were shown to be FADD, while CAP3
and CAP4 remain unidentified(23) . The oligomerized receptor,
along with the associated CAPs, has been designated the DISC (23) . CAP3 or CAP4 are not the recently described candidate
signaling molecules FAP-1 or RIP, as antipeptide antibodies capable of
detecting endogenous FAP-1 or RIP, respectively, were unable to detect
either protein associated with activated or unactivated CD95. ( In conclusion, this is the first
report to functionally establish FADD, one of numerous candidate
signaling molecules, in the proximal signal transduction of CD95. Many
of the contenders, including RIP and FAP1, were not found associated
with the active or inactive receptor, nor are dominant negative
inhibitors likely to exist. Of paramount importance is the fact that
the dominant-negative version of FADD potently abrogates TNF-induced
apoptosis but not TNF-induced NF-
Volume 271,
Number 9,
Issue of March 1, 1996 pp. 4961-4965
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS AND DISCUSSION
FOOTNOTES
ACKNOWLEDGEMENTS
REFERENCES
B activation. FADD-DN bound both receptors, and in
the case of CD95, it disrupted the assembly of a signaling complex.
Taken together, our results functionally establish FADD as the
apoptotic trigger of CD95 and TNFR-1.
)/nerve growth factor receptor family. Activation of
these receptors is caused by aggregation mediated by the respective
ligands or agonist
antibodies(1, 2, 3, 4) . There are
no identifiable catalytic motifs (e.g. kinase or phosphatase)
in the cytoplasmic domains of these cell surface proteins. Instead, it
is becoming apparent that signal transduction is accomplished via
association with an emerging class of novel and diverse signaling
molecules. For example, a dominant-negative mutant of TRAF2 was shown
to block TNFR-2-mediated NF-B activation(5) , while an
analogous mutant of CD40bp (also known as TRAF3, CRAF1, or
LAP1(6, 7, 8) ) was shown to inhibit
CD40-mediated up-regulation of CD23(7) . Numerous candidate
signal transducers have been identified for the two death receptors,
TNFR-1 and CD95, including FADD/MORT1, TRADD, RIP, FAP-1, FAF1, and
TRAP1/2(9, 10, 11, 12, 13) .
Both death receptors share a region of homology of about 80 amino acids
in their cytoplasmic domain required to signal
apoptosis(14, 15) . This shared ``death
domain'' suggests that both receptors engage a common component of
the apoptotic machinery. Here, we investigated the role of FADD in the
proximal signal transduction of CD95 and TNFR-1.
Antibodies and Reagents
The anti-CD95 monoclonal
antibodies used in this study include anti-Fas IgM (Upstate
Biotechnology, Inc.), anti-APO-1 (IgG3,(2) ), and
phosphatidylethanolamine-conjugated anti-Fas (MBL Inc.). Anti-AU1
murine ascites was obtained from Babco, Inc. Anti-PARP antibody was
clone C-2-10, which is described previously (16) , and
recognizes an epitope near the N terminus of PARP located between amino
acids 216 and 375 (generous gift of Dr. G. Poirier). Antibodies were
raised against recombinant GST-FADD fusion protein as described
previously(17) . Rabbit anti-peptide antibodies (Lampire) were
raised against NNKNFHKSTGMTSRSGTD of the p17 subunit of Yama and
STAPGYYSWRNSKDGS of the p12 subunit. C
-ceramide (D-erythro) and C-dihydroceramide (D-erythro) were purchased from Matreya, Inc. and dissolved in
ethanol.Cell Lines and Culture
The B lymphoma cell line
BJAB and the breast carcinoma cell line MCF7 were grown in RPMI 1640
complete medium (10% heat-inactivated fetal bovine serum (Hyclone), L-glutamine, penicillin/streptomycin, and non-essential amino
acids). MCF7-Fas cells, as described previously(18) , were
grown in RPMI 1640 complete media supplemented with 0.5 mg/ml G418
(Life Technologies, Inc.). BJAB and MCF7 stable cell lines were grown
in complete media supplemented with 3 and 0.5 mg/ml G418, respectively. Stable and Transient Transfections
To generate the
pooled stable cell lines, BJAB-FADD-DN and MCF7-FADD-DN, cells were
transfected with pcDNA3-FADD-DN using a protocol described
previously(19) . From the pooled populations, individual clones
were obtained and plated in duplicate on 48-well Costar plates. One set
of cells was treated with anti-Fas IgM (100 ng/ml), and clones
resistant to Fas-induced cell death were identified. The untreated,
resistant clones were then pooled to obtain BJAB-sFADD-DN (which
represents a pool of seven resistant clones) and MCF7-sFADD-DN (which
represents a pool of nine resistant clones). All stable lines generated
were assessed for expression of FADD-DN by immunoblotting. MCF7 cells
were transiently transfected with lipofectamine as described previously (9) .Cell Death and Viability Assays
To assess nuclear
morphology, fluorescent DNA-staining dyes were utilized as described
previously(19) . DNA fragmentation (TUNEL staining) was
determined using the in situ cell death detection kit
(Boehringer Mannheim). BJAB cells were air-dried onto Colorfrost/Plus
microscope slides (Fisher) using 4% paraformaldehyde, and the
manufacturer's protocol was followed. The TUNEL-stained cells
were then counterstained with propidium iodide (10 µg/ml) and
visualized by fluorescence microscopy. To assess cell viability, the
3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide
conversion assay was done on the BJAB cell lines as described
previously(20) .Ceramide Assays
Ceramide levels were determined by
a modified diacylglycerol kinase assay (21, 22) as
described previously (20) .Immunoprecipitations, Western Blotting, and
Two-dimensional Gels
Immunoblotting of cell lysates for PARP was
carried out as described previously(17) . Yama processing was
assessed using 1 
10
BJAB vector and BJAB-sFADD-DN
cells untreated or treated with 100 ng/ml anti-Fas IgM for 18 h. Cells
were then lysed in 60 µl of 0.1% Nonidet P-40, free-thawed three
times, and centrifuged at 14,000 rpm for 20 min. Cytoplasmic extracts
were carefully added to sample buffer and run on a 15% gel, transferred
to a nitrocellulose membrane, and immunoblotted with antibodies
directed against the p17 and p12 subunits of Yama. To show expression
of FADD-DN in BJAB and MCF7 cells, cells were immunoprecipitated in
phosphate-buffered saline-TDS (TDS, 1% Triton X-100, 0.5% deoxycholic
acid, 0.1% SDS) with anti-AU1 antibody (1:100) and Western blotted with
anti-FADD polyclonal antisera (1:1000). Immunoprecipitation of the DISC
and analysis on two-dimensional gels was done as described
previously(23) . Alternatively, cell lysates were
immunoprecipitated with anti-AU1 antibody coupled to protein
A-Sepharose beads as described previously (23) .NF-
MCF7 vector and MCF7-sFADD-DN
cells were transfected with the NF-B AssayB-dependent E-selectin reporter
construct and luciferase activity assessed as described previously (5) .
ceramide (C2), but not
C
-dihydroceramide (DHC2), can bypass the dominant
negative effect of the FADD derivative. The cells characterized include
BJAB vector, BJAB-FADD-DN, and BJAB-sFADD-DN. As a control, cells were
also exposed to the structurally related inactive analog,
C-dihydroceramide (33) . Viabilities were not
decreased significantly, thus validating the specificity of the
cytotoxic effect of C-ceramide. The x axis refers
to the concentration of synthetic ceramide used and the y axis
refers to viability as assessed by 3-(4,5-dimethyl
thiazol-2-yl)-2,5-diphenyl tetrazolium bromide conversion. Viability is
expressed as percentage of vehicle-treated control ± S.E.
Results are representative of three independent experiments. E, CD95-induced activation of the apoptotic protease
Yama/CPP32 is blocked by FADD-DN. BJAB vector and BJAB-sFADD-DN were
left untreated or treated with 100 ng/ml anti-Fas IgM for 18 h. Lysates
were then run on a 15% gel and immunoblotted with polyclonal antibodies
directed against the p17 and p12 subunits of Yama (upper
panel). Cleavage of the death substrate poly(ADP-ribose)
polymerase was also assessed (lower
panel).
-ceramide, confirming that the block in
the death pathway was prior to ceramide generation (Fig. 1D).
converting enzyme (ICE) could
``bypass'' the dominant-negative effect of the FADD
derivative, suggesting that the death pathway was being blocked
upstream of the ICE-like proteases implicated in the apoptotic pathway.
B activation. A, the stable cell lines
utilized include MCF7-sFADD-DN, which represents a pool of nine
resistant clones and a corresponding MCF7 vector control. Expression of
FADD-DN is shown in the left panels. FADD-DN migrates as a
doublet around 18 kDa, possibly due to post-translational modification.
The indicated cell lines were either left untreated (UnRx) or
treated with anti-Fas IgM (250 ng/ml) plus cycloheximide (CHX,
10 µg/ml) or 100 ng/ml TNF for 24 h and stained with propidium
iodide. Similar results were obtained using anti-APO-1 antibody plus
soluble protein A in the absence of cycloheximide (data not shown).
Phase contrast micrographs are shown with corresponding confocal
micrographs (insets) depicting nuclear morphology. B,
MCF7 vector or MCF7-sFADD-DN cells were transfected with an
NF-B-dependent E-selectin-luciferase reporter construct (5) and were either untreated or treated with TNF for 9 h.
Luciferase activities were assessed as described
previously(5) , and values shown are mean ± S.D. of
three independent experiments.
B (NF-B)(30) . We therefore
investigated whether expression of FADD-DN modulated TNF-induced
NF-B activation. MCF7 vector and MCF7-sFADD-DN cells were
transfected with an NF-B-dependent reporter gene (5) and
relative NF-B activity assessed (Fig. 2B). In both
cell lines, NF-B was activated equally well, suggesting that
TNFR-1 utilizes FADD to transduce the death signal and activates
NF-B by a different mechanism.
S]cysteine and
[
S]methionine), lysed with Triton X-100,
immunoprecipitated with anti-APO-1/PA-Sepharose, and subsequently
analyzed by two-dimensional isoelectric focusing, 12%
SDS-polyacrylamide gel electrophoresis. As expected, the four CAPs, as
well as FADD-DN, failed to associate with the unactivated (not
oligomerized) APO-1. However, cells stimulated with anti-APO-1 for 5
min and then lysed show association of the four CAP proteins
with the activated receptor in vector transfected cells. By contrast,
in FADD-DN-expressing cells, FADD-DN associated with the oligomerized
APO-1, while the CAPs did not. The lower left panel is a
schematic illustration of the migration positions of APO-1, CAPs, and
FADD-DN. Large open arrowhead, migration positions of
endogenous FADD (CAP1, CAP2). Large closed arrowhead, FADD-DN. Small open arrowhead, CAP3 (26 kDa) and CAP4 (55 kDa). APO-1
runs as an array of spots around 54 kDa on the basic half of the gel.
FADD-DN was identified in activated sFADD-DN cells by immunoblotting
using anti-AU1 antibody (lower right panel). C, a
model for the role of FADD in the CD95 and TNFR-1 death
pathways.
)As expected, in vector transfected BJAB cells, the DISC
formed upon anti-APO-1 treatment (Fig. 3B). By
contrast, anti-APO-1-stimulated sFADD-DN cells did not form a complete
DISC. Instead, FADD-DN complexed with CD95 in a ligand-dependent
fashion and inhibited the recruitment of FADD (CAP1 and CAP2), CAP3 and
CAP4, thereby disrupting the DISC (Fig. 3B). Similar
results were obtained using FADD-DN expressing MCF7 cells (data not
shown). Thus, our results suggest that the N terminus of FADD, which is
missing in FADD-DN, is required for the recruitment and assembly of the
downstream DISC components, CAP3 and CAP4. Studies are underway to
identify an analagous TNFR-1 DISC.B activation. This suggests that
FADD is the common conduit of the cytokine-mediated death signal and
also demonstrates that the signaling pathways for TNF-induced apoptosis
and NF-B activation are distinct (Fig. 3C). Taken
together, our results demonstrate that FADD is both a necessary and
sufficient mediator of CD95 and TNFR-1-induced apoptosis as
overexpression of FADD engages the cell death machinery (9) ,
while a truncated derivative acts as a potent dominant-negative
regulator. Future studies will hopefully elucidate downstream
components of the pathway, thus linking FADD to the apoptotic proteases
of the ICE/ced-3 family.
)B, nuclear factor-B; ICE, interleukin-1
converting enzyme; TRAF, TNF receptor-associated factor; PARP,
poly(ADP-ribose) polymerase.)
We are grateful to Drs. Yusuf A. Hannun and Supriya
Jayadev for their helpful advice on the ceramide measurements and Dr.
Guy G. Poirier for the anti-PARP antibody. We are thankful to Liandi
Lou, Yongping Kuang, and Uschi Siberzahn for technical assistance and
Ian M. Jones for his expertise in preparing the figures. We thank Kim
Orth and Vidya Sarma for helpful discussions and encouragement.
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
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N. Zampieri, C.-F. Xu, T. A. Neubert, and M. V. Chao Cleavage of p75 Neurotrophin Receptor by {alpha}-Secretase and {gamma}-Secretase Requires Specific Receptor Domains J. Biol. Chem., April 15, 2005; 280(15): 14563 - 14571. [Abstract] [Full Text] [PDF]
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H. Cui, T. Li, and H.-F. Ding Linking of N-Myc to Death Receptor Machinery in Neuroblastoma Cells J. Biol. Chem., March 11, 2005; 280(10): 9474 - 9481. [Abstract] [Full Text] [PDF]
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J. Kuai, J. Wooters, J. P. Hall, V. R. Rao, E. Nickbarg, B. Li, M. Chatterjee-Kishore, Y. Qiu, and L.-L. Lin NAK Is Recruited to the TNFR1 Complex in a TNF{alpha}-dependent Manner and Mediates the Production of RANTES: IDENTIFICATION OF ENDOGENOUS TNFR-INTERACTING PROTEINS BY A PROTEOMIC APPROACH J. Biol. Chem., December 17, 2004; 279(51): 53266 - 53271. [Abstract] [Full Text] [PDF]
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Q. Li, A. K.-K. Ching, B. C.-L. Chan, S. K.-Y. Chow, P.-L. Lim, T. C.-Y. Ho, W.-K. Ip, C.-K. Wong, C. W.-K. Lam, K. K.-H. Lee, et al. A Death Receptor-associated Anti-apoptotic Protein, BRE, Inhibits Mitochondrial Apoptotic Pathway J. Biol. Chem., December 10, 2004; 279(50): 52106 - 52116. [Abstract] [Full Text] [PDF]
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L. Tourneur, S. Delluc, V. Levy, F. Valensi, I. Radford-Weiss, O. Legrand, J. Vargaftig, C. Boix, E. A. Macintyre, B. Varet, et al. Absence or Low Expression of Fas-Associated Protein with Death Domain in Acute Myeloid Leukemia Cells Predicts Resistance to Chemotherapy and Poor Outcome Cancer Res., November 1, 2004; 64(21): 8101 - 8108. [Abstract] [Full Text] [PDF]
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V. M. Abrahams, P. Bole-Aldo, Y. M. Kim, S. L. Straszewski-Chavez, T. Chaiworapongsa, R. Romero, and G. Mor Divergent Trophoblast Responses to Bacterial Products Mediated by TLRs J. Immunol., October 1, 2004; 173(7): 4286 - 4296. [Abstract] [Full Text] [PDF]
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K. Ruckdeschel, G. Pfaffinger, R. Haase, A. Sing, H. Weighardt, G. Hacker, B. Holzmann, and J. Heesemann Signaling of Apoptosis through TLRs Critically Involves Toll/IL-1 Receptor Domain-Containing Adapter Inducing IFN-{beta}, but Not MyD88, in Bacteria-Infected Murine Macrophages J. Immunol., September 1, 2004; 173(5): 3320 - 3328. [Abstract] [Full Text] [PDF]
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L. R. Thomas, A. Henson, J. C. Reed, F. R. Salsbury, and A. Thorburn Direct Binding of Fas-associated Death Domain (FADD) to the Tumor Necrosis Factor-related Apoptosis-inducing Ligand Receptor DR5 Is Regulated by the Death Effector Domain of FADD J. Biol. Chem., July 30, 2004; 279(31): 32780 - 32785. [Abstract] [Full Text] [PDF]
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H. M. Beere `The stress of dying': the role of heat shock proteins in the regulation of apoptosis J. Cell Sci., June 1, 2004; 117(13): 2641 - 2651. [Abstract] [Full Text] [PDF]
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E. Kurenova, L.-H. Xu, X. Yang, A. S. Baldwin Jr., R. J. Craven, S. K. Hanks, Z.-g. Liu, and W. G. Cance Focal Adhesion Kinase Suppresses Apoptosis by Binding to the Death Domain of Receptor-Interacting Protein Mol. Cell. Biol., May 15, 2004; 24(10): 4361 - 4371. [Abstract] [Full Text] [PDF]
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K. R. Mills, M. Reginato, J. Debnath, B. Queenan, and J. S. Brugge Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is required for induction of autophagy during lumen formation in vitro PNAS, March 9, 2004; 101(10): 3438 - 3443. [Abstract] [Full Text] [PDF]
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D. R. Wesemann and E. N. Benveniste STAT-1{alpha} and IFN-{gamma} as Modulators of TNF-{alpha} Signaling in Macrophages: Regulation and Functional Implications of the TNF Receptor 1:STAT-1{alpha} Complex J. Immunol., November 15, 2003; 171(10): 5313 - 5319. [Abstract] [Full Text] [PDF]
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N. Harper, M. A. Hughes, S. N. Farrow, G. M. Cohen, and M. MacFarlane Protein Kinase C Modulates Tumor Necrosis Factor-related Apoptosis-inducing Ligand-induced Apoptosis by Targeting the Apical Events of Death Receptor Signaling J. Biol. Chem., November 7, 2003; 278(45): 44338 - 44347. [Abstract] [Full Text] [PDF]
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E. C. Alappat, J. Volkland, and M. E. Peter Cell Cycle Effects by C-FADD Depend on Its C-terminal Phosphorylation Site J. Biol. Chem., October 24, 2003; 278(43): 41585 - 41588. [Abstract] [Full Text] [PDF]
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R. Haase, C. J. Kirschning, A. Sing, P. Schrottner, K. Fukase, S. Kusumoto, H. Wagner, J. Heesemann, and K. Ruckdeschel A Dominant Role of Toll-Like Receptor 4 in the Signaling of Apoptosis in Bacteria-Faced Macrophages J. Immunol., October 15, 2003; 171(8): 4294 - 4303. [Abstract] [Full Text] [PDF]
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N. Harper, M. Hughes, M. MacFarlane, and G. M. Cohen Fas-associated Death Domain Protein and Caspase-8 Are Not Recruited to the Tumor Necrosis Factor Receptor 1 Signaling Complex during Tumor Necrosis Factor-induced Apoptosis J. Biol. Chem., July 3, 2003; 278(28): 25534 - 25541. [Abstract] [Full Text] [PDF]
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M. Maksimow, M. Santanen, S. Jalkanen, and A. Hanninen Responding naive T cells differ in their sensitivity to Fas engagement: early death of many T cells is compensated by costimulation of surviving T cells Blood, May 15, 2003; 101(10): 4022 - 4028. [Abstract] [Full Text] [PDF]
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B. F. Yang, C. Xiao, W. H. Roa, P. H. Krammer, and C. Hao Calcium/Calmodulin-dependent Protein Kinase II Regulation of c-FLIP Expression and Phosphorylation in Modulation of Fas-mediated Signaling in Malignant Glioma Cells J. Biol. Chem., February 21, 2003; 278(9): 7043 - 7050. [Abstract] [Full Text] [PDF]
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J. Luo, Y. Sun, H. Lin, Y. Qian, Z. Li, S. S. Leonard, C. Huang, and X. Shi Activation of JNK by Vanadate Induces a Fas-associated Death Domain (FADD)-dependent Death of Cerebellar Granule Progenitors in Vitro J. Biol. Chem., February 7, 2003; 278(7): 4542 - 4551. [Abstract] [Full Text] [PDF]
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L. M. Frago, S. Canon, E. J. de la Rosa, Y. Leon, and I. Varela-Nieto Programmed cell death in the developing inner ear is balanced by nerve growth factor and insulin-like growth factor I J. Cell Sci., February 1, 2003; 116(3): 475 - 486. [Abstract] [Full Text] [PDF]
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P. Shankaranarayanan and S. Nigam IL-4 Induces Apoptosis in A549 Lung Adenocarcinoma Cells: Evidence for the Pivotal Role of 15-Hydroxyeicosatetraenoic Acid Binding to Activated Peroxisome Proliferator-Activated Receptor {gamma} Transcription Factor J. Immunol., January 15, 2003; 170(2): 887 - 894. [Abstract] [Full Text] [PDF]
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P. Ducoroy, O. Micheau, S. Perruche, L. Dubrez-Daloz, D. de Fornel, P. Dutartre, P. Saas, and E. Solary LF 15-0195 immunosuppressive agent enhances activation-induced T-cell death by facilitating caspase-8 and caspase-10 activation at the DISC level Blood, January 1, 2003; 101(1): 194 - 201. [Abstract] [Full Text] [PDF]
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K. Rosen, W. Shi, B. Calabretta, and J. Filmus Cell Detachment Triggers p38 Mitogen-activated Protein Kinase-dependent Overexpression of Fas Ligand. A NOVEL MECHANISM OF ANOIKIS OF INTESTINAL EPITHELIAL CELLS J. Biol. Chem., November 22, 2002; 277(48): 46123 - 46130. [Abstract] [Full Text] [PDF]
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P. K. M. Kim, Y. Wang, A. Gambotto, Y.-M. Kim, R. Weller, B. S. Zuckerbraun, Y. Hua, S. C. Watkins, and T. R. Billiar Hepatocyte Fas-associating Death Domain Protein/Mediator of Receptor-induced Toxicity (FADD/MORT1) Levels Increase in Response to Pro-apoptotic Stimuli J. Biol. Chem., October 4, 2002; 277(41): 38855 - 38862. [Abstract] [Full Text] [PDF]
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V. Golubovskaya, L. Beviglia, L.-H. Xu, H. S. Earp III, R. Craven, and W. Cance Dual Inhibition of Focal Adhesion Kinase and Epidermal Growth Factor Receptor Pathways Cooperatively Induces Death Receptor-mediated Apoptosis in Human Breast Cancer Cells J. Biol. Chem., October 4, 2002; 277(41): 38978 - 38987. [Abstract] [Full Text] [PDF]
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L. R. Thomas, D. J. Stillman, and A. Thorburn Regulation of Fas-associated Death Domain Interactions by the Death Effector Domain Identified by a Modified Reverse Two-hybrid Screen J. Biol. Chem., September 6, 2002; 277(37): 34343 - 34348. [Abstract] [Full Text] [PDF]
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K.-L. He and A. T. Ting A20 Inhibits Tumor Necrosis Factor (TNF) Alpha-Induced Apoptosis by Disrupting Recruitment of TRADD and RIP to the TNF Receptor 1 Complex in Jurkat T Cells Mol. Cell. Biol., September 1, 2002; 22(17): 6034 - 6045. [Abstract] [Full Text] [PDF]
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W. Chao, Y. Shen, L. Li, and A. Rosenzweig Importance of FADD Signaling in Serum Deprivation- and Hypoxia-induced Cardiomyocyte Apoptosis J. Biol. Chem., August 23, 2002; 277(35): 31639 - 31645. [Abstract] [Full Text] [PDF]
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B. Munz, E. Hildt, M. L. Springer, and H. M. Blau RIP2, a Checkpoint in Myogenic Differentiation Mol. Cell. Biol., August 15, 2002; 22(16): 5879 - 5886. [Abstract] [Full Text] [PDF]
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B. Liu, D. Peng, Y. Lu, W. Jin, and Z. Fan A Novel Single Amino Acid Deletion Caspase-8 Mutant in Cancer Cells That Lost Proapoptotic Activity J. Biol. Chem., August 9, 2002; 277(33): 30159 - 30164. [Abstract] [Full Text] [PDF]
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D. Himeji, T. Horiuchi, H. Tsukamoto, K. Hayashi, T. Watanabe, and M. Harada Characterization of caspase-8L: a novel isoform of caspase-8 that behaves as an inhibitor of the caspase cascade Blood, May 13, 2002; 99(11): 4070 - 4078. [Abstract] [Full Text] [PDF]
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D. Chen, X. Li, Z. Zhai, and H.-B. Shu A Novel Zinc Finger Protein Interacts with Receptor-interacting Protein (RIP) and Inhibits Tumor Necrosis Factor (TNF)- and IL1-induced NF-kappa B Activation J. Biol. Chem., May 3, 2002; 277(18): 15985 - 15991. [Abstract] [Full Text] [PDF]
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M. Bond, G. Murphy, M. R. Bennett, A. C. Newby, and A. H. Baker Tissue Inhibitor of Metalloproteinase-3 Induces a Fas-associated Death Domain-dependent Type II Apoptotic Pathway J. Biol. Chem., April 12, 2002; 277(16): 13787 - 13795. [Abstract] [Full Text] [PDF]
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L. Roz, M. Gramegna, H. Ishii, C. M. Croce, and G. Sozzi Restoration of fragile histidine triad (FHIT) expression induces apoptosis and suppresses tumorigenicity in lung and cervical cancer cell lines PNAS, March 19, 2002; 99(6): 3615 - 3620. [Abstract] [Full Text] [PDF]
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P. Chu, D. Deforce, I. M. Pedersen, Y. Kim, S. Kitada, J. C. Reed, and T. J. Kipps Latent sensitivity to Fas-mediated apoptosis after CD40 ligation may explain activity of CD154 gene therapy in chronic lymphocytic leukemia PNAS, March 19, 2002; 99(6): 3854 - 3859. [Abstract] [Full Text] [PDF]
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D. D. Bannerman, J. C. Tupper, R. D. Erwert, R. K. Winn, and J. M. Harlan Divergence of Bacterial Lipopolysaccharide Pro-apoptotic Signaling Downstream of IRAK-1 J. Biol. Chem., March 1, 2002; 277(10): 8048 - 8053. [Abstract] [Full Text] [PDF]
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X. W. Meng, M. P. Heldebrant, and S. H. Kaufmann Phorbol 12-myristate 13-Acetate Inhibits Death Receptor-mediated Apoptosis in Jurkat Cells by Disrupting Recruitment of Fas-associated Polypeptide with Death Domain J. Biol. Chem., January 25, 2002; 277(5): 3776 - 3783. [Abstract] [Full Text] [PDF]
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C. Kumar-Sinha, S. Varambally, A. Sreekumar, and A. M. Chinnaiyan Molecular Cross-talk between the TRAIL and Interferon Signaling Pathways J. Biol. Chem., January 4, 2002; 277(1): 575 - 585. [Abstract] [Full Text]
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A. Algeciras-Schimnich, L. Shen, B. C. Barnhart, A. E. Murmann, J. K. Burkhardt, and M. E. Peter Molecular Ordering of the Initial Signaling Events of CD95 Mol. Cell. Biol., January 1, 2002; 22(1): 207 - 220. [Abstract] [Full Text] [PDF]
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I. Herr and K.-M. Debatin Cellular stress response and apoptosis in cancer therapy Blood, November 1, 2001; 98(9): 2603 - 2614. [Abstract] [Full Text] [PDF]
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D. G. Stupack, X. S. Puente, S. Boutsaboualoy, C. M. Storgard, and D. A. Cheresh Apoptosis of adherent cells by recruitment of caspase-8 to unligated integrins J. Cell Biol., October 29, 2001; 155(3): 459 - 470. [Abstract] [Full Text] [PDF]
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D. Chatterjee, I. Schmitz, A. Krueger, K. Yeung, S. Kirchhoff, P. H. Krammer, M. E. Peter, J. H. Wyche, and P. Pantazis Induction of Apoptosis in 9-Nitrocamptothecin-treated DU145 Human Prostate Carcinoma Cells Correlates with de Novo Synthesis of CD95 and CD95 Ligand and Down-Regulation of c-FLIPshort Cancer Res., October 1, 2001; 61(19): 7148 - 7154. [Abstract] [Full Text] [PDF]
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A. Sreekumar, M. K. Nyati, S. Varambally, T. R. Barrette, D. Ghosh, T. S. Lawrence, and A. M. Chinnaiyan Profiling of Cancer Cells Using Protein Microarrays: Discovery of Novel Radiation-regulated Proteins Cancer Res., October 1, 2001; 61(20): 7585 - 7593. [Abstract] [Full Text] [PDF]
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J. Wipasa, H. Xu, A. Stowers, and M. F. Good Apoptotic Deletion of Th Cells Specific for the 19-kDa Carboxyl-Terminal Fragment of Merozoite Surface Protein 1 During Malaria Infection J. Immunol., October 1, 2001; 167(7): 3903 - 3909. [Abstract] [Full Text] [PDF]
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S. Gilbert, A. Loranger, N. Daigle, and N. Marceau Simple epithelium keratins 8 and 18 provide resistance to Fas-mediated apoptosis. The protection occurs through a receptor-targeting modulation J. Cell Biol., August 20, 2001; 154(4): 763 - 774. [Abstract] [Full Text] [PDF]
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L. Besnault, N. Schrantz, M. T. Auffredou, G. Leca, M. F. Bourgeade, and A. Vazquez B Cell Receptor Cross-Linking Triggers a Caspase-8- Dependent Apoptotic Pathway That Is Independent of the Death Effector Domain of Fas-Associated Death Domain Protein J. Immunol., July 15, 2001; 167(2): 733 - 740. [Abstract] [Full Text] [PDF]
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I. M. Catlett, P. Xie, B. S. Hostager, and G. A. Bishop Signaling Through MHC Class II Molecules Blocks CD95-Induced Apoptosis J. Immunol., May 15, 2001; 166(10): 6019 - 6024. [Abstract] [Full Text] [PDF]
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T. Wieder, F. Essmann, A. Prokop, K. Schmelz, K. Schulze-Osthoff, R. Beyaert, B. Dorken, and P. T. Daniel Activation of caspase-8 in drug-induced apoptosis of B-lymphoid cells is independent of CD95/Fas receptor-ligand interaction and occurs downstream of caspase-3 Blood, March 1, 2001; 97(5): 1378 - 1387. [Abstract] [Full Text] [PDF]
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D.-W. Seol, J. Li, M.-H. Seol, S.-Y. Park, R. V. Talanian, and T. R. Billiar Signaling Events Triggered by Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL): Caspase-8 Is Required for TRAIL-induced Apoptosis Cancer Res., February 1, 2001; 61(3): 1138 - 1143. [Abstract] [Full Text]
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R. K. Rathbun, T. A. Christianson, G. R. Faulkner, G. Jones, W. Keeble, M. O'Dwyer, and G. C. Bagby Interferon-gamma -induced apoptotic responses of Fanconi anemia group C hematopoietic progenitor cells involve caspase 8-dependent activation of caspase 3 family members Blood, December 15, 2000; 96(13): 4204 - 4211. [Abstract] [Full Text] [PDF]
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N. Droin, M. Beauchemin, E. Solary, and R. Bertrand Identification of a Caspase-2 Isoform that Behaves as an Endogenous Inhibitor of the Caspase Cascade Cancer Res., December 1, 2000; 60(24): 7039 - 7047. [Abstract] [Full Text]
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S. Kirchhoff, W. W. Muller, A. Krueger, I. Schmitz, and P. H. Krammer TCR-Mediated Up-Regulation of c-FLIPshort Correlates with Resistance Toward CD95-Mediated Apoptosis by Blocking Death-Inducing Signaling Complex Activity J. Immunol., December 1, 2000; 165(11): 6293 - 6300. [Abstract] [Full Text] [PDF]
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N. Embade, P. F. Valerón, S. Aznar, E. López-Collazo, and J. C. Lacal Apoptosis Induced by Rac GTPase Correlates with Induction of FasL and Ceramides Production Mol. Biol. Cell, December 1, 2000; 11(12): 4347 - 4358. [Abstract] [Full Text]
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A. D. Badley, A. A. Pilon, A. Landay, and D. H. Lynch Mechanisms of HIV-associated lymphocyte apoptosis Blood, November 1, 2000; 96(9): 2951 - 2964. [Abstract] [Full Text] [PDF]
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J. W. Ramos, P. E. Hughes, M. W. Renshaw, M. A. Schwartz, E. Formstecher, H. Chneiweiss, and M. H. Ginsberg Death Effector Domain Protein PEA-15 Potentiates Ras Activation of Extracellular Signal Receptor-activated Kinase by an Adhesion-independent Mechanism Mol. Biol. Cell, September 1, 2000; 11(9): 2863 - 2872. [Abstract] [Full Text]
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M. Li and A. A. Beg Induction of Necrotic-Like Cell Death by Tumor Necrosis Factor Alpha and Caspase Inhibitors: Novel Mechanism for Killing Virus-Infected Cells J. Virol., August 15, 2000; 74(16): 7470 - 7477. [Abstract] [Full Text]
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S. Fulda, E. Meyer, and K.-M. Debatin Metabolic Inhibitors Sensitize for CD95 (APO-1/Fas)-induced Apoptosis by Down-Regulating Fas-associated Death Domain-like Interleukin 1-Converting Enzyme Inhibitory Protein Expression Cancer Res., July 1, 2000; 60(14): 3947 - 3956. [Abstract] [Full Text]
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D.-W. Seol and T. R. Billiar Cysteine 230 Modulates Tumor Necrosis Factor-related Apoptosis-inducing Ligand Activity Cancer Res., June 1, 2000; 60(12): 3152 - 3154. [Abstract] [Full Text]
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C. Beltinger, S. Fulda, T. Kammertoens, W. Uckert, and K.-M. Debatin Mitochondrial Amplification of Death Signals Determines Thymidine Kinase/Ganciclovir-triggered Activation of Apoptosis Cancer Res., June 1, 2000; 60(12): 3212 - 3217. [Abstract] [Full Text]
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E. Hatano, C. A. Bradham, A. Stark, Y. Iimuro, J. J. Lemasters, and D. A. Brenner The Mitochondrial Permeability Transition Augments Fas-induced Apoptosis in Mouse Hepatocytes J. Biol. Chem., April 14, 2000; 275(16): 11814 - 11823. [Abstract] [Full Text] [PDF]
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W.-H. Hu, H. Johnson, and H.-B. Shu Activation of NF-kappa B by FADD, Casper, and Caspase-8 J. Biol. Chem., April 6, 2000; 275(15): 10838 - 10844. [Abstract] [Full Text] [PDF]
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D. J. Brick, R. D. Burke, A. A. Minkley, and C. Upton Ectromelia virus virulence factor p28 acts upstream of caspase-3 in response to UV light-induced apoptosis J. Gen. Virol., April 1, 2000; 81(4): 1087 - 1097. [Abstract] [Full Text]
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A.-O. Hueber, M. Zornig, A.-M. Bernard, M. Chautan, and G. Evan A Dominant Negative Fas-associated Death Domain Protein Mutant Inhibits Proliferation and Leads to Impaired Calcium Mobilization in Both T-cells and Fibroblasts J. Biol. Chem., March 31, 2000; 275(14): 10453 - 10462. [Abstract] [Full Text] [PDF]
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C. Grullich, M. C. Sullards, Z. Fuks, A. H. Merrill Jr., and R. Kolesnick CD95(Fas/APO-1) Signals Ceramide Generation Independent of the Effector Stage of Apoptosis J. Biol. Chem., March 17, 2000; 275(12): 8650 - 8656. [Abstract] [Full Text] [PDF]
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T. Lin, L. Genestier, M. J. Pinkoski, A. Castro, S. Nicholas, R. Mogil, F. Paris, Z. Fuks, E. H. Schuchman, R. N. Kolesnick, et al. Role of Acidic Sphingomyelinase in Fas/CD95-mediated Cell Death J. Biol. Chem., March 17, 2000; 275(12): 8657 - 8663. [Abstract] [Full Text] [PDF]
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