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BCL2 — FAS
Text-mined interactions from Literome
Fernandez et al., Dev Dyn 2001
:
Bax and
Fas , proapoptotic proteins, were
detected homogeneously throughout both ventricles in the neonate, while
Bcl-2 , an antiapoptotic protein, was not detectable
van der Kolk et al., Leukemia 2002
(Burkitt Lymphoma) :
Lastly,
Bcl-2 overexpression blocked cyt-c release and the decrease in Deltapsi ( m ), and completely
prevented CD95- or BCR mediated apoptosis ; however, it did not affect CD20XL induced cell death
Tung et al., Am J Physiol Heart Circ Physiol 2003
:
These changes in the
Fas-Fas ligand pathway and
Bcl-2 mitochondrial apoptosis
regulation are enhanced by complete suppression of antiapoptotic FADD-like IL-1beta converting enzyme inhibitory protein ( FLIP ) ( from 30.5 to 0.0 %, P < 0.01 ) and Bcl-xL ( from 22.5 to 0.1 %, P = 0.03 ) expression among these cells from the earliest days after gene transfer
Almawi et al., J Leukoc Biol 2004
:
The antagonism of apoptosis afforded by prosurvival Bcl-2 proteins appeared to be specific for the GCs, as
Bcl-2 and Bcl-x ( L ) blocked GC-induced apoptosis in T cell hybridomas but did not
affect Fas or activation induced apoptosis
Hua et al., J Immunol 2005
:
Effects of
Bcl-2 levels on
Fas signaling induced caspase-3 activation : molecular genetic tests of computational model predictions
Yuan et al., Mitochondrion 2001
:
Using a stable transfected CEM cell line, we show that
Bcl-2 suppressed caspase processing in both cytosolic and mitochondrial compartments in
response to both staurosporine and
Fas ligation
Bilim et al., Br J Cancer 2008
(Carcinoma, Renal Cell...) :
Compared to the parental and mock transfected cells, neither clone was more sensitive to conventional chemotherapeutic agents, but both clones were more susceptible to
Fas stimulation ( P < 0.0001 ) and to pharmacological
Bcl-2 inhibition ( P < 0.0001 ), as well as to a combination of the two ( P < 0.0001 )
Fan et al., Amino Acids 2009
:
Taken together, the findings of this study have demonstrated that L-carnitine could induce apoptosis in hepa1c1c7 cells by regulating
Fas ligands and
inhibiting the expression of
Bcl-2
Li et al., Sheng Li Xue Bao 2010
(Atherosclerosis) :
As shown in our preliminary study, MCP-1 induced apoptosis of hUVECs in a dose dependent manner at both 24 h and 48 h. FACS and Western blot analysis results in the present study indicated that MCP-1 promoted the expression of proapoptotic proteins Bax and
Fas and
inhibited the expression of antiapoptotic protein
Bcl-2
Mazumdar et al., Cancer Res 2011
(Colonic Neoplasms) :
Thus, activated GLI genes repress DR5 and Fas expressions while upregulating
Bcl-2 and PDGFRa expressions to
inhibit Fas and facilitate cell survival
Wu et al., Environ Toxicol 2013
:
Western blot analysis demonstrated that propofol promoted
Fas , cytochrome c, caspase-9 and -3 active form and Bax levels, but
inhibited Bcl-xl protein level which led to cell apoptosis
Wu et al., Nan Fang Yi Ke Da Xue Xue Bao 2011
(Brain Ischemia...) :
To investigate the
effect of
Bcl-2 overexpression on
Fas and TNFR1 mediated apoptosis and its possible mechanism in rat hippocampus following global ischemia/reperfusion ( IR )
Mandal et al., J Biol Chem 1996
:
Bcl-2 prevents
CD95 ( Fas/APO-1 ) -induced degradation of lamin B and poly ( ADP-ribose ) polymerase and restores the NF-kappaB signaling pathway
Gougeon et al., J Immunol 1997
(Chronic Disease...) :
Interestingly, in contrast to the situation found in infected humans,
Fas ligation by agonistic Abs or recombinant human Fas ligand on CD4 and CD8 T cells from infected chimpanzees did not
induce apoptosis in these subsets even when
Bcl-2 was down-regulated
BrĂ¡s et al., J Immunol 1997
(Lymphoma, B-Cell) :
In this system,
Fas ligation also
triggers Bcl-2/Bcl-x down-regulation, an effect inhibited by sIgG cross linking, the cysteine protease inhibitor acetyl-Tyr-Val-Ala-Asp-chloromethyl ketone, and PMA treatment ... In A20 cells,
Fas signaling may thus
trigger both ICE activation and Bcl-x and
Bcl-2 down-regulation
Srinivasan et al., J Biol Chem 1998
(Breast Neoplasms) :
Bcl-xL functions downstream of caspase-8 to
inhibit Fas- and tumor necrosis factor receptor 1-induced apoptosis of MCF7 breast carcinoma cells ... In some cells,
Bcl-xL overexpression can
inhibit anti-Fas- and tumor necrosis factor (TNF)-alpha induced apoptosis
Wakisaka et al., Clin Exp Immunol 1998
(Arthritis, Rheumatoid) :
Anti-Fas MoAb induced apoptosis of RA synovial cells in vitro, and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and IL-1beta, but not IL-6 or IL-8,
inhibited the anti-Fas induced apoptosis accompanying up-regulation of
Bcl-2 protein expression and reduced expression of CPP32 and ICH-1L. Immunohistochemical study revealed that CPP32 and ICH-1L were expressed weakly in the RA synovial lining cells compared with osteoarthritis ( OA ) synovial lining cells
Fulda et al., Cancer Res 1998
(Neuroblastoma) :
After Doxo treatment, enhanced
CD95/CD95-L expression and caspase-8 activation were not
blocked by
Bcl-2 or Bcl-X ( L ) and were found in cells with a mitochondrial transmembrane potential ( delta psi ( m ) ) that was still normal ( delta psi ( m ) high cells )