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The Journal of biological chemistry, 276(42), 38610-38618 (2001-08-17)
Toxic bile salts induce hepatocyte apoptosis by both Fas-dependent and -independent mechanisms. In this study, we examined the cellular mechanisms responsible for Fas-independent, bile acid-mediated apoptosis. HuH-7 cells, which are known to be Fas deficient, were stably transfected with the
The bile salts chenodeoxycholate (CDC) and its 7 beta-hydroxy epimer ursodeoxycholate (UDC) are administered therapeutically (as acids) to dissolve cholesterol gallstones in man. Since their micellarr solutions and those of their physiological conjugates differ strikingly in their capacities to solubilize
Biochimica et biophysica acta, 1805(2), 123-140 (2009-12-08)
Formation of the pro-apoptotic death-inducing signaling complex (DISC) can be initiated in cancer cells via binding of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) to its two pro-apoptotic receptors, TRAIL receptor 1 (TRAIL-R1) and TRAIL-R2. Primary components of the DISC are
Inducible nitric oxide synthase (iNOS) and nitric oxide (NO) can ameliorate apoptosis induced by toxic glycochenodeoxycholate (GCDC) in hepatocytes. However, the underlying molecular mechanisms are not yet understood in detail. This study is to clarify the function of iNOS/NO and
Journal of hepatology, 55(1), 133-144 (2010-12-15)
Reactive oxygen species (ROS) and nitric oxide (NO) exert a relevant role during bile acid-induced hepatotoxicity. Whether α-Tocopherol regulates oxidative and nitrosative stress, bile acid transporter expression and their NO-dependent post-translational modifications, and cell death were assessed in vitro and
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