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Molecular biology of the cell
Jul, 2007;18 (7): 2630-5.

Depletion of the nucleolar protein nucleostemin causes G1 cell cycle arrest via the p53 pathway.

Hanhui Ma, Thoru Pederson
Author Information
  1. Hanhui Ma: Program in Cell Dynamics, Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
PMID: 17494866 DOI: 10.1091/mbc.e07-03-0244

Abstract

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, and how it participates in cell growth regulation. Here, we show that NS is down-regulated by the tumor suppressor p14(ARF) 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 small interfering RNA knockdown. These results demonstrate that, in the cells investigated, the level of NS is regulated by p14(ARF) and the control of the G1/S transition by NS operates in a p53-dependent manner.

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MeSH Term

ADP-Ribosylation Factors
Carrier Proteins
Cell Nucleolus
Down-Regulation
G1 Phase
GTP-Binding Proteins
HeLa Cells
Humans
Nuclear Proteins
Proto-Oncogene Proteins c-mdm2
Retinoblastoma Protein
Tumor Suppressor Protein p53
Up-Regulation

Chemicals

Carrier Proteins
GNL3 protein, human
Nuclear Proteins
Retinoblastoma Protein
Tumor Suppressor Protein p53
MDM2 protein, human
Proto-Oncogene Proteins c-mdm2
GTP-Binding Proteins
ADP-Ribosylation Factors
Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Word Cloud

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