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FASLG — JUN
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Kolbus et al., Mol Cell Biol 2000
:
c-Jun dependent
CD95-L expression is a rate limiting step in the induction of apoptosis by alkylating agents
Harwood et al., J Biol Chem 2000
(Colonic Neoplasms) :
Regulation of
FasL by NF-kappaB and
AP-1 in Fas dependent thymineless death of human colon carcinoma cells ... These results demonstrate the crucial
roles for NF-kappaB and
AP-1 in the regulation of
FasL in Fas mediated thymineless death of colon carcinoma cells
Villunger et al., J Immunol 2000
:
Fas ligand induced
c-Jun kinase activation in lymphoid cells requires extensive receptor aggregation but is independent of DAXX, and Fas mediated cell death does not involve DAXX, RIP, or RAIDD
Ghose et al., Cancer Res 2001
(Carcinoma, Squamous Cell...) :
This was confirmed by the fact that exogenous expression of a dominant negative deletion mutant of
c-Jun ( TAM67 )
reduced the induction of both apoptosis and
Fas-L by SDG
Suhara et al., Mol Cell Biol 2002
:
Similarly, induction of
FasL by the Akt regulated forkhead transcription factor FKHRL1 was
dependent upon caspase and
c-Jun activation
Tomicic et al., Mol Pharmacol 2003
(Necrosis) :
The findings also show that the drug causes the induction of
c-Jun and the activation of activator protein-1 resulting in increased
level of
Fas ligand (FasL) and caspase-8/-3 activation
Su et al., Carcinogenesis 2005
:
These results suggest the possible
involvement of apoptosis signal regulating kinase
1/c-Jun N-terminal kinase signaling in the regulation of
FasL expression and subsequent apoptosis induced by resveratrol in HL-60 cells
Imamura et al., J Biol Chem 2004
(Inflammation) :
Reporter gene assays involving wild-type and mutated IL-8 promoters and NF-kappaB- and AP-1 reporter constructs indicated that an
FasL induced NF-kappaB and
AP-1 activity are required for maximal promoter activity
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
Trauzold et al., FASEB J 2005
(Adenocarcinoma...) :
Stimulation of TRAF2 overexpressing cells with
CD95 ligand led to induction of NF-kappaB and
AP-1 , enhanced IL-8- and uPA-secretion, and a further increased invasiveness
Kuo et al., Chem Biol Interact 2005
(Disease Models, Animal) :
CS triggered activation of MAP kinase ( p38/JNK or ERK2 ) pathway, which led to
Jun or p53 phosphorylation and
FasL induction links Fas phosphorylation
Matsumoto et al., FEBS J 2007
(MAP Kinase Signaling System) :
Here, we found that a dominant negative mutant of c-Jun, a component of the activator protein-1 (AP-1) transcription factor, inhibits
FasL induced
AP-1 activity and IL-8 production in HEK293 cells ... The
FasL induced
AP-1 activation could be inhibited by deleting or introducing the lymphoproliferation ( lpr ) -type point mutation into the Fas death domain ( DD ), knocking down the Fas associated DD protein (FADD), abrogating caspase-8 expression with small interfering RNAs, or using inhibitors for pan-caspase and caspase-8 but not caspase-1 or caspase-3 ... Furthermore, wildtype, but not a catalytically inactive mutant, of caspase-8 reconstituted the
FasL induced
AP-1 activation in caspase-8-deficient cells ... Unexpectedly, an inhibitor for JNK but not for MAPK/ERK kinase inhibited the
FasL induced
AP-1 activation and IL-8 production ... These results demonstrate that
FasL induced
AP-1 activation is required for optimal IL-8 production, and this process is mediated by FADD, caspase-8, and JNK
Ma et al., J Biol Chem 2007
:
Here, we showed that the up-regulation of dp5, but not
fas ligand and bim, after potassium deprivation was
suppressed by the expression of a dominant negative form of
c-Jun
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
Faris et al., Mol Cell Biol 1998
:
While the mechanism by which stress stimuli induce apoptosis is not well understood, we have previously shown that the induction of
Fas ligand (FasL) gene expression by environmental stress stimuli is
dependent on
c-Jun N-terminal kinase (JNK) activation
Le-Niculescu et al., Mol Cell Biol 1999
:
JNK activation detected by
c-Jun phosphorylation and
FasL induction are also observed after removal of either nerve growth factor from differentiated PC12 cells or KCl from primary cerebellar granule neurons ( CGCs )