Mechanisms in TGF-ß action Journal Article
| Authors: | Massagué, J.; Heino, J.; Laiho, M. |
| Article Title: | Mechanisms in TGF-ß action |
| Abstract: | The various isoforms of TGF-beta are multifunctional. We are exploring pathways of cellular regulation by TGF-beta that lead to suppression of cell proliferation, modulation of cell adhesion and control of cell differentiation. These cellular responses appear to be activated by binding of TGF-beta to a similar set of receptor glycoproteins in all cell types. TGF-beta receptor types I and II are specifically lost in cell mutants that are resistant to TGF-beta. The concomitant loss of these two receptors in certain mutants suggests that they are components of the TGF-beta signal-transducing receptor complex. Inhibition of epithelial cell proliferation by TGF-beta is linked to retention of the retinoblastoma growth suppressor gene product in an underphosphorylated state that is presumed to have growth suppressive activity. Inhibition of myogenic differentiation by TGF-beta involves a block in the expression of the master myogenic differentiation genes, such as myogenin, but appears also to involve up-regulation of extracellular matrix production. Expression of components of the cell adhesion apparatus-cell adhesion receptors and extracellular matrix proteins-is controlled by TGF-beta in an array of cell types. This response could have a great impact on the ability of cells to migrate, home to specific tissue locations and differentiate during development, invasion and metastasis. |
| Keywords: | extracellular-matrix; adhesion; receptors; myogenic differentiation; susceptibility gene; transforming growth-factor; retinoblastoma protein-phosphorylation; osteo-sarcoma cells; selective loss; cycle regulatory element |
| Journal Title: | Ciba Foundation Symposia |
| Volume: | 157 |
| ISSN: | 0300-5208 |
| Publisher: | John Wiley & Sons |
| Date Published: | 1991-01-01 |
| Start Page: | 51 |
| End Page: | 59; discussion 59-65 |
| Language: | English |
| ACCESSION: | WOS:A1991GD85100004 |
| PROVIDER: | wos |
| PUBMED: | 1649037 |
| DOI: | 10.1002/9780470514061.ch4 |
| Notes: | Article -- Source: Wos |
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