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Am J Physiol Renal Physiol 277: F186-F194, 1999;
0363-6127/99 $5.00
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Vol. 277, Issue 2, F186-F194, August 1999

TGF-beta 1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase

Baolian Liu and Patricia Preisig

Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75235-8856

When renal epithelial cells are exposed to epidermal growth factor-transforming growth factor-beta 1 (EGF-TGF-beta 1) the typical EGF-mediated hyperplastic growth response is converted to a hypertrophic growth response. Hypertrophy in this setting involves cell entrance into G1, but arrest of cell cycle progression at the G1/S interface. Late G1 arrest is mediated by retaining retinoblastoma protein (pRB) in its active, hypophosphorylated state. The present studies examine the mechanism by which pRB is retained in its active state. The results demonstrate that TGF-beta 1-mediated conversion of hyperplasia to hypertrophy involves preventing activation of cdk2/cyclin E kinase but has no effect on cdk4(6)/cyclin D kinase activity. Preventing activation of cyclin E kinase is associated with 1) decreased abundance of cdk2/cyclin E complexes and 2) retention of p57Kip2 in formed cdk2/cyclin E complexes. The development of hypertrophy does not involve regulation of either cdk2, cyclin E, or cdc25A protein abundances, or the abundance of p27Kip1 or p21 in formed complexes.

kidney; cell cycle; cell growth; cyclin kinase inhibitors; G1 kinases


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