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Munshi et al., J Immunol 2002
:
LPS also
augmented expression of the pro-apoptotic protein
Bax and the tumor suppressor gene p53
Fukui et al., J Immunol 2003
:
LPS stimulation
induced the expression of Fas, caspase 8, cellular FLIP Bfl-1/A1, and Bcl-x, but not FasL, TNFR p55, Bak,
Bax , and Bad at the transcriptional level
Souvannavong et al., Infect Immun 2004
:
Unlike staurosporine,
LPS induced the retention of
Bax , a proapoptotic protein of the Bcl-2 family, in the cytosol by preventing its translocation to mitochondria
Sano et al., Res Vet Sci 2005
:
By real-time quantitative PCR analysis, it was indicated that Bcl-xL and
Bax levels in canine neutrophils were significantly
affected by
LPS stimulation
Ramana et al., Free Radic Biol Med 2007
:
In addition, AR inhibition prevented the
LPS induced down-regulation of Bcl-xl and up-regulation of
Bax and Bak in macrophages
Bonior et al., J Physiol Pharmacol 2007
(Endotoxemia) :
In spite of this observations the
effects of
LPS and caerulein on pro-apoptotic HSP60 and
Bax protein expression in the pancreatic acinar cells has not been examined yet
Sharifi et al., Toxicol Mech Methods 2010
:
In western blotting analysis,
LPS ( 200 microg/ml ) also
enhanced expression of pro-apoptotic
Bax and pro-caspase-3 proteins compared to controls, while the expression of Bcl-2 protein was not changed significantly ... From the present results, it might be concluded that
LPS can
cause PC12 cell death, in which apoptosis plays an important role, possibly by the mitochondrial pathway through higher expression of the
Bax as well as caspase 3 protein
Takeuchi et al., Arch Oral Biol 2011
(Gingival Overgrowth) :
The levels of
Bax and cytochrome c proteins in NIFr were not
up-regulated by
LPS compared with NIFn
Aggarwal et al., Frontiers in physiology 2012
:
Finally, our studies showed that
LPS induced an increase in the mitochondrial translocation of
Bax , caspase 3 activation, and nuclear DNA fragmentation and these parameters were all prevented with GSH-EE