TGF-β1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase

American Journal of Physiology - Renal Physiology

Volumn 277, Issue 2 46-2, 1999, Pages

  Liu, Baolian ^a   Preisig, Patricia ^a  

^a UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

Author keywords

Cell cycle; Cell growth; Cyclin kinase inhibitors; G1 kinases; Kidney

Indexed keywords

CELL CYCLE PROTEIN; CYCLIN DEPENDENT KINASE; CYCLIN E; CYCLIN E KINASE; PHOSPHOTRANSFERASE; PROTEIN P21; PROTEIN P27; RETINOBLASTOMA PROTEIN; TRANSFORMING GROWTH FACTOR BETA1; UNCLASSIFIED DRUG; CDC25A PROTEIN; CDK2 PROTEIN, RAT; CDK4 PROTEIN, RAT; CDKN1B PROTEIN, RAT; CYCLIN DEPENDENT KINASE 2; CYCLIN DEPENDENT KINASE 4; CYCLIN DEPENDENT KINASE INHIBITOR 1B; CYCLIN DEPENDENT KINASE INHIBITOR 1C; CYCLIN E DEPENDENT KINASE; CYCLIN E-DEPENDENT KINASE; EPIDERMAL GROWTH FACTOR; MICROTUBULE ASSOCIATED PROTEIN; NUCLEAR PROTEIN; ONCOPROTEIN; PROTEIN SERINE THREONINE KINASE; PROTEIN TYROSINE PHOSPHATASE; TRANSFORMING GROWTH FACTOR BETA; TUMOR SUPPRESSOR PROTEIN;

ANIMAL CELL; ARTICLE; CELL CYCLE; ENZYME ACTIVATION; ENZYME ACTIVITY; ENZYME INHIBITION; HYPERPLASIA; KIDNEY EPITHELIUM; KIDNEY HYPERTROPHY; NONHUMAN; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; RAT; REGULATORY MECHANISM; ANIMAL; CELL LINE; CYTOLOGY; DRUG ANTAGONISM; DRUG EFFECT; HYPERTROPHY; KIDNEY; METABOLISM; PATHOLOGY; PHOSPHORYLATION;

ANIMALS; CDC2-CDC28 KINASES; CDC25 PHOSPHATASE; CELL CYCLE PROTEINS; CELL LINE; CYCLIN-DEPENDENT KINASE 2; CYCLIN-DEPENDENT KINASE 4; CYCLIN-DEPENDENT KINASE INHIBITOR P27; CYCLIN-DEPENDENT KINASE INHIBITOR P57; CYCLIN-DEPENDENT KINASES; ENZYME ACTIVATION; EPIDERMAL GROWTH FACTOR; HYPERTROPHY; KIDNEY; MICROTUBULE-ASSOCIATED PROTEINS; NUCLEAR PROTEINS; PHOSPHORYLATION; PROTEIN-SERINE-THREONINE KINASES; PROTEIN-TYROSINE-PHOSPHATASE; PROTO-ONCOGENE PROTEINS; RATS; RETINOBLASTOMA PROTEIN; TRANSFORMING GROWTH FACTOR BETA; TUMOR SUPPRESSOR PROTEINS;

EID: 0033173308     PISSN: 1931857X     EISSN: 15221466     Source Type: Journal    
DOI: 10.1152/ajprenal.1999.277.2.f186     Document Type: Article

References (32)

1. Bradford, M. M. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal. Biochem. 72: 243-245, 1976.
2. Connell-Crowley, L., J. W. Harper, and D. W. Goodrich. Cyclin D1/cdk4 regulates retinoblastoma protein-mediated cell cycle arrest by site-specific phosphorylation. Mol. Biol. Cell 8: 287-301, 1997.
3. Deshaies, R. J. Phosphorylation and proteolysis: partners in the regulation of cell division in budding yeast. Curr. Opin. Genet. Dev. 7: 7-16, 1997.
4. Ezhevsky, S. A., H. Nagahara, A. M. Vocero-Akbani, D. R. Gius, M. C. Wei, and S. F. Dowdy. Hypo-phosphorylation of the retinoblastoma protein (pRB) by cyclin D: cdk4/6 complexes results in active pRb. Proc. Natl. Acad. Sc. USA 94: 10699-10704, 1997.
5. Fine, L. G., J. T. Norman, D. A. Kujubu, and A. Knecht. Renal hypertrophy. In: The Kidney: Physiology and Pathophysiology, edited by D. W. Selden and G. Giebish. New York: Raven, 1992, p. 3113-3133.
6. Fisher, R. P. CDKs and cyclins in transition(s). Curr. Opin. Genet. Dev. 7: 32-38, 1997.
7. 4Cl-induced hypertrophy is mediated by weak base effects and is independent of cell cycle processes. Am. J. Physiol. 270 (Cell Physiol. 39): C932-C938, 1996.
8. Franch, H. A., J. W. Shay, R. J. Alpern, and P. A. Preisig. Involvement of pRB family in TGFB-dependent epithelial cell hypertrophy. J. Cell Biol. 129: 245-254, 1995.
9. Galaktionov, K., X. Chen, and D. Beach. Cdc25 cell-cycle phosphatase as a target of c-myc. Nature 382: 511-517, 1996.
10. Ginsberg, D., G. Vairo, T. Chittenden, Z. X. Xiao, G. Xu, K. L. Wydner, J. A. DeCaprio, J. B. Lawrence, and D. M. Livingston. E2F-4, a new member of the E2F transcription factor family, interacts with p107. Genes Dev. 8: 2665-2679, 1994.
11. Gu, Y., J. Rosenblatt, and D. O. Morgan. Cell cycle regulation of CDK2 activity by phosphorylation of Thr160 and Tyr15. EMBO J. 11: 3995-4005, 1992.
12. 1/S transition. EMBO J. 13: 4302-4310, 1994.
13. Huang, H.-C., and P. A. Preisig. Cyclin D kinase is activated in all diabetic renal growth, while cyclin E kinase determines whether the growth pattern will be hyperplasia or hypertrophy. (Abstract). J. Am Soc. Nephrol. 9: 440A, 1998.
14. Iavarone, A., and J. Massague. Repression of the CDK activator Cdc25A and cell-cycle arrest by cytokine TGF-β in cells lacking the CDK inhibitor p15. Nature 387: 417-422, 1997.
15. Jinno, S., K. Suto, A. Nagata, M. Igarashi, Y. Kanaoka, H. Nojima, and H. Okayama. Cdc25A is a novel phosphatase functioning early in the cell cycle. EMBO J. 13: 1549-1556, 1994.
16. Kitagawa, M., H. Higashi, H.-K. Jung, I. Suzukitakahashi, M. Ikeda, K. Tamai, J. Kato, K. Segawa, E. Yoshida, S. Nishimura, and Y. Taya. The consensus motif for phosphorylation by cyclin D1-cdk4 is different from that for phosphorylation by cyclin A/E-cdk2. EMBO J. 15: 7060-7069, 1996.
17. 1 in mammalian cells: inhibition of cyclin E-dependent kinase by TGF-β. Science 260: 536-539, 1993.
18. LaBaer, J., M. D. Garrett, L. F. Stevenson, J. M. Slingerland, C. Sandhu, H. S. Chou, A. Fattaey, and E. Harlow. New functional activities for the p21 family of CDK inhibitors. Genes Dev. 11: 847-862, 1997.
19. Lew, D. J., and S. Kornbluth. Regulatory roles of cyclin dependent kinase phosphorylation in cell cycle control. Curr. Opin. Cell Biol. 8: 795-804, 1996.
20. Liu, B., and P. A. Preisig. Compensatory renal hypertrophy (CRH) is mediated by both cell cycle-dependent and -independent growth processes (Abstract). J. Am. Soc. Nephrol. 9: 444A, 1998.
21. Lundberg, A. S., and R. A. Weinberg. Functional inactivation of the retinoblastoma protein requires sequential modification by at least two distinct cyclin-cdk complexes. Mol. Cell. Biol. 18: 753-761, 1998.
22. Morgan, D. O. The dynamics of cyclin dependent kinase structure. Curr. Opin. Cell Biol. 8: 767-772, 1996.
23. Norman, J. T., and L. G. Fine. Renal growth and hypertrophy. In: Textbook of Nephrology, edited by S. G. Massry and R. J. Glassock. Baltimore: Williams & Wilkins, 1995, p. 146-158.
24. Pagano, M., R. Pepperkok, F. Verde, W. Ansorge, and G. Draetta. Cyclin A is required at two points in the human cell cycle. EMBO J. 11: 961-971, 1992.
25. Preisig, P. A., and H. A. Franch. Renal epithelial cell hyperplasia and hypertrophy. Semin. Nephrol. 15: 327-340, 1995.
26. 1 and E with an inducible system. Mol. Cell. Biol. 14: 1669-1679, 1994.
27. Shankland, S. J. Cell-cycle control and renal disease. Kidney Int. 52: 294-308, 1997.
28. 1 cyclin-dependent kinases. Genes Dev. 9: 1149-1163, 1995.
29. 0-like arrest. Mol. Cell. Biol. 16: 3934-3944, 1996.
30. Wolf, G., and E. G. Neilson. Molecular mechanisms of tubulointerstitial hypertrophy and hyperplasia. Kidney Int. 39: 401-420, 1991.
31. KiP1. Kidney Int. 50: 2112-2119, 1996.
32. Zhang, H., G. J. Hannon, and D. Beach. p21-containing cyclin kinases exist in both active and inactive states. Genes Dev. 8: 1750-1758, 1994.