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Science 3 November 1989:
Vol. 246. no. 4930, pp. 603 - 608
DOI: 10.1126/science.2683075

Articles

Science, Vol 246, Issue 4930, 603-608
Copyright © 1989 by American Association for the Advancement of Science


articles

G1 events and regulation of cell proliferation

AB Pardee

Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA.

Cells prepare for S phase during the G1 phase of the cell cycle. Cell biological methods have provided knowledge of cycle kinetics and of substages of G1 that are determined by extracellular signals. Through the use of biochemical and molecular biological techniques to study effects of growth factors, oncogenes, and inhibitors, intracellular events during G1 that lead to DNA synthesis are rapidly being discovered. Many cells in vivo are in a quiescent state (G0), with unduplicated DNA. Cells can be activated to reenter the cycle during G1. Similarly, cells in culture can be shifted between G0 and G1. These switches in and out of G1 are the main determinants of post-embryonic cell proliferation rate and are defectively controlled in cancer cells.


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   Abstract »    Full Text »    PDF »
The Lack of Cyclin Kinase Inhibitor p27Kip1 Ameliorates Progression of Diabetic Nephropathy.
M. Awazu, S. Omori, K. Ishikura, M. Hida, and H. Fujita (2003)
J. Am. Soc. Nephrol. 14, 699-708
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Loss of Protooncogene c-Myc Function Impedes G1 Phase Progression Both before and after the Restriction Point.
C. Schorl and J. M. Sedivy (2003)
Mol. Biol. Cell 14, 823-835
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Transduction of Growth or Mitogenic Signals into Translational Activation of TOP mRNAs Is Fully Reliant on the Phosphatidylinositol 3-Kinase-Mediated Pathway but Requires neither S6K1 nor rpS6 Phosphorylation.
M. Stolovich, H. Tang, E. Hornstein, G. Levy, R. Cohen, S. S. Bae, M. J. Birnbaum, and O. Meyuhas (2002)
Mol. Cell. Biol. 22, 8101-8113
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Clonal Anergy Is Maintained Independently of T Cell Proliferation.
S. Colombetti, F. Benigni, V. Basso, and A. Mondino (2002)
J. Immunol. 169, 6178-6186
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Cdk4 disruption renders primary mouse cells resistant to oncogenic transformation, leading to Arf/p53-independent senescence.
X. Zou, D. Ray, A. Aziyu, K. Christov, A. D. Boiko, A. V. Gudkov, and H. Kiyokawa (2002)
Genes & Dev. 16, 2923-2934
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Ca2+/calmodulin-dependent and cAMP-dependent kinases in induction of c-fos in human mesangial cells.
H. Zeng, Y. Liu, and D. M. Templeton (2002)
Am J Physiol Renal Physiol 283, F888-F894
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Inhibition of Bcl-XL Phosphorylation by Tea Polyphenols or Epigallocatechin-3-Gallate Is Associated with Prostate Cancer Cell Apoptosis.
A. Kazi, D. M. Smith, Q. Zhong, and Q. P. Dou (2002)
Mol. Pharmacol. 62, 765-771
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Dihydrotestosterone Inhibits Granulosa Cell Proliferation by Decreasing the Cyclin D2 mRNA Expression and Cell Cycle Arrest at G1 Phase.
P. K. Pradeep, X. Li, H. Peegel, and K. M. J. Menon (2002)
Endocrinology 143, 2930-2935
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Pituitary Hypoplasia and Lactotroph Dysfunction in Mice Deficient for Cyclin-Dependent Kinase-4.
D. S. Moons, S. Jirawatnotai, A. F. Parlow, G. Gibori, R. D. Kineman, and H. Kiyokawa (2002)
Endocrinology 143, 3001-3008
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3,3'-Diindolylmethane (DIM) induces a G1 cell cycle arrest in human breast cancer cells that is accompanied by Sp1-mediated activation of p21WAF1/CIP1 expression.
C. Hong, Hyeon.-A. Kim, G. L. Firestone, and L. F. Bjeldanes (2002)
Carcinogenesis 23, 1297-1305
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