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FAS — JUN
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
FAS
→
Complex of JUN-STAT3
(decreases)
Evidence: Downregulation of FAS expression is a common event during tumor progression and has been correlated with resistance to radiation or drug-induced cell death. Importantly, STAT3 binds directly to the FAS promoter in association with JUN to suppress the transcription of the death receptor.
Text-mined interactions from Literome
Abreu-Martin et al., Am J Physiol 1999
:
Signaling through
Fas results in activation of JNK and
AP-1 binding activity that is increased in the presence of IFN-gamma
Low et al., Oncogene 1999
:
Fas ligation in the presence of cycloheximide
induced Jun N-terminal kinase 1 (JNK1) and JNK2 phosphorylation, caspase activation and cell death in the IL-3 dependent cell line BAF3
Chen et al., Oncogene 1999
:
Activation of
c-Jun N-terminal kinase (JNK) by
Fas ligation is caspase dependent, suggesting that caspases may regulate activators of the JNK pathway
Bernassola et al., J Cell Biochem 2001
:
Cross linking of CD95 enhanced AP-1 DNA binding activity and
AP-1 dependent
CD95L transactivation, which were both significantly reduced by different NO-donors compounds
Afford et al., FASEB J 2001
(Liver Cirrhosis, Biliary) :
CD40 activation induced,
Fas dependent apoptosis and
NF-kappaB/AP-1 signaling in human intrahepatic biliary epithelial cells
Ivanov et al., J Biol Chem 2002
:
Regulation of
Fas expression by STAT3 and
c-Jun is mediated by phosphatidylinositol 3-kinase-AKT signaling
Cariers et al., Cell Physiol Biochem 2002
:
CHX induced a transient and
CD95L a delayed
activation of
c-Jun-N-terminal kinase (JNK) , but when added together initial JNK activation was enhanced and prolonged
Galvan et al., J Biol Chem 2003
:
Apoptosis signal regulating kinase 1 ( ASK1 ) is a MAP kinase kinase kinase ( MAPKKK ) that is required for
c-Jun N-terminal kinase (JNK) and p38 activation in
response to
Fas and tumor necrosis factor (TNF) receptor stimulation, and for oxidative stress- and TNFalpha induced apoptosis
Baumann et al., Oncogene 2003
:
Ectopic expression of transdominant negative
Jun mutants strongly
reduced CD95L promoter activity and activation induced cell death ( AICD ), confirming the functional significance of FosB/c-Jun binding
Peng et al., Toxicol Appl Pharmacol 2005
(Glioma) :
The result reveals that ( AC ) ( 5 ) GP induces JNK activation and
c-Jun phosphorylation thus
stimulating the expression of Fas-L and
Fas
Kim et al., FEBS J 2008
(Uterine Cervical Neoplasms) :
In addition, dominant negative form of
c-Jun inhibited radiation induced
Fas expression and Bax and Bak activation
Chen et al., J Cell Biochem 2009
(Calcium Signaling...) :
Together with the previous finding that
c-Jun and ATF-2 are
involved in transcriptional regulation of
Fas and FasL, our data suggest that PLA(2) induces Fas and FasL upregulation through p38 alpha MAPK/ATF-2 and JNK1/c-Jun pathways in K562 cells, and PLA(2) catalytic activity is involved in this action
Chen et al., J Cell Physiol 2010
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
Knock-down of c-Fos and c-Jun protein expression by siRNA suggested that c-Fos counteracted the
effect of
c-Jun on
Fas/FasL up-regulation
Machida et al., Hepatology 2010
(Carcinoma, Hepatocellular...) :
The core protein also suppresses apoptosis mediated by Fas ligand because of
c-Jun dependent
Fas down-regulation
Latinis et al., Blood 1996
(Leukemia-Lymphoma, Adult T-Cell) :
Fas ligation
induces apoptosis and
Jun kinase activation independently of CD45 and Lck in human T cells ... Further, in normal and CD45- or Lck-deficient cell lines,
Fas stimulation
results in activation of
Jun kinase (JNK) , a proposed mediator of stress activation pathways
Wilson et al., Eur J Immunol 1996
(Lymphoma) :
Rather,
Fas ligation strongly
activates Jun kinase (JNK)