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Originally published In Press as doi:10.1074/jbc.M007411200 on December 15, 2000

J. Biol. Chem., Vol. 276, Issue 11, 7932-7936, March 16, 2001
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Interaction between YY1 and the Retinoblastoma Protein
REGULATION OF CELL CYCLE PROGRESSION IN DIFFERENTIATED CELLS*

Viktoria PetkovaDagger , Michael J. Romanowski§, Indra SulijoadikusumoDagger , Daniela RohneDagger , Peter KangDagger , Thomas Shenk§, and Anny UshevaDagger ||

From the Dagger  Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachuttes 02215 and the § Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544

Overexpression of the transcription factor YY1 activates DNA synthesis in differentiated primary human coronary artery smooth muscle cells. Overexpression of the retinoblastoma protein together with YY1 blocked this effect. In growth-arrested cells, YY1 resides in a complex with the retinoblastoma protein, but the complex is not detected in serum-stimulated S phase cultures, indicating that the interaction of the retinoblastoma protein and YY1 is cell cycle-regulated. Recombinant retinoblastoma protein directly interacts with YY1, destabilizing the interaction of YY1 with DNA and inhibiting its transcription initiator function in vitro. We conclude that in differentiated cells elevation of the nuclear level of YY1 protein favors progression into the S phase, and we propose that this activity is regulated by its interaction with the retinoblastoma protein.


* This work was supported by National Institutes of Health Grants HL62458 (to A. U.) and CA38965 (to T. S.) and grants from the American Heart Association (to A. U.) and the Edward Mallinckrodt, Jr. Foundation (to A. U.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Present address: The Rockefeller University, 1230 York Ave., New York, NY 10021.

|| To whom correspondence should be addressed: Div. of Endocrinology, Dept. of Medicine, Beth Israel Deconess Medical Center, Harvard Medical School, 99 Brookline Ave., R313, Boston, MA 02215. Tel.: 617-632-0522; Fax: 617-667-2927; E-mail: ausheva@caregroup.harvard.edu.


Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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