Transforming growth factor beta effects on expression of G1 cyclins and cyclin-dependent protein kinases

Transforming growth factor beta 1 (TGF-beta 1) is a potent growth-inhibitory polypeptide. The mechanism of TGF-beta 1 inhibition has been related to its ability to prevent the hyperphosphorylation of retinoblastoma protein (pRb). Several lines of evidence have suggested that cell cycle-regulated pro...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1993-11, Vol.90 (21), p.10315-10319
Main Authors: YAN GENG, WEINBERG, R. A
Format: Article
Language:English
Subjects:
Biological and medical sciences
Blotting, Northern
Cell Cycle - drug effects
Cell cycle, cell proliferation
Cell Line
Cell physiology
Cyclins - biosynthesis
DNA Replication - drug effects
Fundamental and applied biological sciences. Psychology
G1 Phase - drug effects
Humans
Keratinocytes - cytology
Keratinocytes - drug effects
Keratinocytes - metabolism
Kinetics
Molecular and cellular biology
Protein Kinases - biosynthesis
RNA - isolation & purification
RNA - metabolism
Time Factors
Transforming Growth Factor beta - pharmacology
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Summary:Transforming growth factor beta 1 (TGF-beta 1) is a potent growth-inhibitory polypeptide. The mechanism of TGF-beta 1 inhibition has been related to its ability to prevent the hyperphosphorylation of retinoblastoma protein (pRb). Several lines of evidence have suggested that cell cycle-regulated protein kinases are responsible for the hyperphosphorylation of pRb. We demonstrate here that TGF-beta 1 has profound effects on the expression of genes encoding certain G1 cyclins and their associated kinases, which provides one explanation of TGF-beta 1 effects on pRb hyperphosphorylation. These results also suggest that the growth-inhibitory effects of TGF-beta 1 in many cells are attributable to its effects on the cell cycle apparatus involved in programming G1 transit.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.90.21.10315