FASEB J. Thermo Fisher Scientific
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pistoi, S.
Right arrow Articles by Morello, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pistoi, S.
Right arrow Articles by Morello, D.

The FASEB Journal, Vol 10, 819-828, Copyright © 1996 by The Federation of American Societies for Experimental Biology

REVIEWS

Liver regeneration 7. Prometheus' myth revisited: transgenic mice as a powerful tool to study liver regeneration

S Pistoi and D Morello
Department of Immunology, Institut Pasteur, Paris, France.

In this review, we present examples of the contribution of transgenic mice to our knowledge concerning the type of cells that are able to repopulate a damaged liver and information on the factors and mechanisms involved in postnatal liver growth and regeneration. The transgenic technology offers the opportunity to evaluate the physiological consequences of perturbating expression of a given gene in vivo. It has provided insights into the concerted action of extracellular (HGF/SF, TGF-alpha, EGF, TGF-beta) and intracellular factors (c-myc, c-fos, c-jun, p53, c-met, and others) in liver regeneration. Transgenic mice can also contribute to the dissection of the molecular mechanisms responsible for the regulated expression of these factors, both at the transcriptional and the posttranscriptional level. An illustration of such a strategy is given by the study of the sequences involved in the posttranscriptional regulation of the c-myc proto-oncogene. The recent improvement of gene targeting, in which endogenous genes are inactivated by homologous recombination, represents a further step toward the study of the function of a particular gene. Inactivation of most of the factors described in this review has been undertaken. However, further studies of their role in liver growth control are impeded by the fact that the corresponding knockout mice die prematurely. This problem could be overcome by the advent of new techniques, which will be briefly presented, aimed at turning genes on and off at will and in a tissue-specific manner.


This article has been cited by other articles:


Home page
 Cancer Res.Home page
F. Li, Y. Xiang, J. Potter, R. Dinavahi, C. V. Dang, and L. A. Lee
Conditional Deletion of c-myc Does Not Impair Liver Regeneration
Cancer Res., June 1, 2006; 66(11): 5608 - 5612.
[Abstract] [Full Text] [PDF]

Home page
 Exp. Biol. Med.Home page
J.-L. Liu, S. Yakar, and D. LeRoith
Conditional Knockout of Mouse Insulin-Like Growth Factor-1 Gene Using the Cre/loxP System
Experimental Biology and Medicine, April 1, 2000; 223(4): 344 - 351.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 by The Federation of American Societies for Experimental Biology.