AJP - GI Add DOIs to your references at manuscript stage!
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 284: G734-G738, 2003; doi:10.1152/ajpgi.00491.2002
0193-1857/03 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (40)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Higuchi, H.
Right arrow Articles by Gores, G. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Higuchi, H.
Right arrow Articles by Gores, G. J.
Vol. 284, Issue 5, G734-G738, May 2003

THEME
Bile Acid Regulation of Hepatic Physiology
IV. Bile acids and death receptors

Hajime Higuchi and Gregory J. Gores

Division of Gastroenterology and Hepatology, Mayo Medical School, Clinic, and Foundation, Rochester, Minnesota 55905

Toxic bile acids facilitate Fas and tumor necrosis factor-associated apoptosis-inducing ligand (TRAIL) death-receptor oligomerization and activation. Bile acid modulation of death-receptor signaling is multifactorial and includes trafficking of Fas to the cell surface, enhancing TRAIL-R2/DR5 expression, and suppression of function of cFLIP, an antiapoptotic protein modulating death-receptor function. Because bile acid-associated death receptor-mediated apoptosis is a common mechanism for cholestatic hepatocyte injury, inhibition of death receptors and their cascades may prove useful in attenuating liver injury during cholestasis.

Fas; tumor necrosis factor-associated apoptosis-inducing ligand; Bid


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
R. E. Castro, J. D. Amaral, S. Sola, B. T. Kren, C. J. Steer, and C. M. P. Rodrigues
Differential regulation of cyclin D1 and cell death by bile acids in primary rat hepatocytes
Am J Physiol Gastrointest Liver Physiol, July 1, 2007; 293(1): G327 - G334.
[Abstract] [Full Text] [PDF]

Home page
 J BiochemHome page
S. Yui, T. Saeki, R. Kanamoto, and K. Iwami
Characteristics of Apoptosis in HCT116 Colon Cancer Cells Induced by Deoxycholic Acid
J. Biochem., August 1, 2005; 138(2): 151 - 157.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
K. A. Cullen, J. McCool, M. S. Anwer, and C. R. L. Webster
Activation of cAMP-guanine exchange factor confers PKA-independent protection from hepatocyte apoptosis
Am J Physiol Gastrointest Liver Physiol, August 1, 2004; 287(2): G334 - G343.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
M. J. Czaja
The Future of GI and Liver Research: Editorial Perspectives: III. JNK/AP-1 regulation of hepatocyte death
Am J Physiol Gastrointest Liver Physiol, June 1, 2003; 284(6): G875 - G879.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online