Distinct mechanisms control genome recognition by p53 at its target genes linked to different cell fates.

Marina Farkas, Department of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA, United States
Hideharu Hashimoto, ThomaDepartment of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA, United States
Ramana V Davuluri, Northwestern University Feinberg School of Medicine, Chicago, IL, United States
Lois Resnick-Silverman, Icahn School of Medicine at Mount Sinai, New York, NY, United States
James J Manfredi, Icahn School of Medicine at Mount Sinai, New York, NY, United States
Erik W. Debler, Department of Biochemistry and Molecular Biology, Thomas Jefferson University, Philadelphia, PA, United States
Steven B McMahon, Department of Cancer Biology, Thomas Jefferson University; Kimmel Cancer Center, Thomas Jefferson University
Yingtao Bi, Northwestern University Feinberg School of Medicine, Chicago, IL, United States

Document Type Article

This article has been peer reviewed. It was published in: Nature Communications.

2021 Jan 20;12(1):484.

The published version is available at DOI: 10.1038/s41467-020-20783-z

Copyright © 2021, The Author(s).

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Abstract

The tumor suppressor p53 integrates stress response pathways by selectively engaging one of several potential transcriptomes, thereby triggering cell fate decisions (e.g., cell cycle arrest, apoptosis). Foundational to this process is the binding of tetrameric p53 to 20-bp response elements (REs) in the genome (RRRCWWGYYYN