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BAX — FAS

Text-mined interactions from Literome

Kobayashi et al., Cell Death Differ 1998 : The Bax gene was activated in irradiated and ara-C treated BV173 cells, but Fas/APO-1 was induced only in irradiated BV173 cells
Inoue et al., Hum Cell 2001 (Neoplasms) : A Bax induces apoptosis mitochondria-dependently, whereas Fas can induce apoptosis mitochondria-independently
Wang et al., J Biol Chem 2003 : In human KB epithelial cells expressing the caspase-resistant mutant crBAP31, Fas stimulation resulted in cleavage of BID and insertion of BAX into mitochondrial membrane, but subsequent oligomerization of BAX and BAK, egress of cytochrome c to the cytosol, and apoptosis were impaired
Moodley et al., Am J Respir Cell Mol Biol 2003 (MAP Kinase Signaling System...) : Using RNase protection assays, we showed that IL-6 enhanced Fas induced apoptosis and expression of Bax in normal-Fb, but inhibited apoptosis and induced expression of Bcl-2 in IPF-Fb. Densitometry of Western blots revealed a Bcl-2/Bax ratio 0.15 +/- 0.01 in normal-Fb compared with 12.05 +/- 1.0 in IPF-Fb. Upregulation of Bcl-2 in normal-Fb and Bax in IPF-Fb were both STAT-3 dependent
Wei et al., Mol Reprod Dev 2005 : Modest Fas staining with no obvious change was detected throughout the menstrual cycle, while the levels of FasL and Bax protein in the epithelial cells increased in the secretory phase when apoptosis was most prevalent
Kim et al., FEBS J 2008 (Uterine Cervical Neoplasms) : These results indicate that the JNK-c-Jun pathway is required for the transcriptional upregulation of Fas and subsequent activation of Bax and Bak, and that JNK, but not c-Jun, is directly associated with phosphorylation and downregulation of Bcl-2 in response to ionizing radiation
Chang et al., J Biol Chem 2009 : These findings suggest that Fas mediate SPE B-induced Bax expression through p38
Yoo et al., Int J Nanomedicine 2012 : In this study, we demonstrated that combined treatment with TiO ( 2 ) nanoparticles sized less than 100 nm and ultraviolet A irradiation induces apoptotic cell death through reactive oxygen species dependent upregulation of Fas and conformational activation of Bax in normal human cells
Egle et al., Br J Haematol 1997 (Multiple Myeloma) : In conclusion, our results suggest a p53 independent co-regulation of Apo-1/Fas and Bax, as well as a role for Bax in Apo-1/Fas induced apoptosis in myeloma