TY - JOUR
AU - 
AB - THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 275, No. 50, Issue of December 15, pp. 39458 –39465, 2000 © 2000 by The American Society for Biochemistry and Molecular Biology, Inc. Printed in U.S.A. DIFFERENTIAL ROLE OF PROLIFERATING CELL NUCLEAR ANTIGEN* Received for publication, July 25, 2000, and in revised form, September 6, 2000 Published, JBC Papers in Press, September 7, 2000, DOI 10.1074/jbc.M006626200 ¶ i Kenichi Fujise‡§ , Di Zhang‡, Juinn-lin Liu , and Edward T. H. Yeh‡§ From the ‡Research Center for Cardiovascular Diseases, Institute of Molecular Medicine for Prevention of Human Diseases, §Divisions of Cardiology and Molecular Medicine, Department of Internal Medicine, University of Texas Health Science Center, Houston, and Department of Neuro-oncology, M. D. Anderson Cancer Center, Houston, Texas 77030 ating cell nuclear antigen (PCNA) (1). On the other hand, the MCL1 (ML1 myeloid cell leukemia 1), a Bcl-2 (B- cell lymphoma-leukemia 2) homologue, is known to function activation of bax, noxa, fas, and p53-inducible genes causes as an anti-apoptotic protein. Here we show in vitro and cells to undergo apoptosis (2–5). Although the exact mechanism in vivo that MCL1 interacts with the cell cycle regulator, by which p53 preferentially activates genes related to either proliferating cell 
TI - Regulation of Apoptosis and Cell Cycle Progression by MCL1
JF - Journal of Biological Chemistry
DO - 10.1074/jbc.m006626200
DA - 2000-12-01
UR - https://www.deepdyve.com/lp/unpaywall/regulation-of-apoptosis-and-cell-cycle-progression-by-mcl1-d2G0v0nBwP
DP - DeepDyve
ER -