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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)