HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Roger, P. P Search for Related Content PubMed Articles by Roger, P. P

Thyrotropin-dependent transforming growth factor beta expression in thyroid gland

Normal cell proliferation is controlled by a balance between positive and negative intracellular and extracellular signals. Transforming growth factor beta (i.e. three closely related isoforms TGF-β1, TGF-β2 and TGFβ3) is the most potent extracellular growth inhibitor for a wide variety of cell types in vitro and in vivo, including selected cell types of mesenchymal and myeloid origin, as well as nearly all epithelial, lymphoid and endothelial cells (1). Nevertheless, by stimulating an autocrine pathway. TGF-β is a potent "indirect" mitogen for a few mesenchymal cell types. The molecular mechanisms by which TGF-β inhibits epithelial cell cycle progression, and how many carcinoma cells lose responsiveness to TGF-β inhibition, are currently areas of major interest (1). On the other hand, TGF-β is also a multifunctional cytokine with diverse biological actions, which influences a wide range of cellular, physiological, immunological and developmental processes (2, 3). Expression of TGF-β precursor mRNA has been detected

This article has been cited by other articles:

				F. Depoortere, I. Pirson, J. Bartek, J. E. Dumont, and P. P. Roger Transforming Growth Factor beta 1 Selectively Inhibits the Cyclic AMP-dependent Proliferation of Primary Thyroid Epithelial Cells by Preventing the Association of Cyclin D3-cdk4 with Nuclear p27kip1 Mol. Biol. Cell, March 1, 2000; 11(3): 1061 - 1076. [Abstract] [Full Text]