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MBC in Press, published online ahead of print May 9, 2007
Mol. Biol. Cell 10.1091/mbc.E07-03-0244

A more recent version of this article appeared on July 1, 2007
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Submitted on March 16, 2007
Revised on April 19, 2007
Accepted on April 26, 2007

Depletion of the Nucleolar Protein Nucleostemin Causes G1 Cell Cycle Arrest via the p53 Pathway

Hanhui Ma and Thoru Pederson

Program in Cell Dynamics and Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605

Monitoring Editor: Mark Solomon

Nucleostemin (NS) is a nucleolar protein expressed in adult and embryo-derived stem cells, transformed cell lines and tumors. NS decreases when proliferating cells exit the cell cycle but it is unknown how NS is controlled on the one hand, and how it participates in cell growth regulation on the other. Here we show that NS is down-regulated by the tumor suppressor p14ARF, and that NS knockdown elevates the level of tumor suppressor p53. NS knockdown led to G1 cell-cycle arrest in p53-positive cells but not in cells in which p53 was genetically deficient or depleted by siRNA knockdown. These results demonstrate that, in the cells investigated, the level of NS is regulated by ARF and the control of the G1/S transition by NS operates in a p53-dependent manner.

Address correspondence to: Thoru Pederson (thoru.pederson{at}umassmed.edu)




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