USF-LVHN SELECT
Frame-shift mediated reduction of gain-of-function p53 R273H and deletion of the R273H C-terminus in breast cancer cells result in replication-stress sensitivity.
Publication/Presentation Date
6-8-2021
Abstract
We recently documented that gain-of-function (GOF) mutant p53 (mtp53) R273H in triple negative breast cancer (TNBC) cells interacts with replicating DNA and PARP1. The missense R273H GOF mtp53 has a mutated central DNA binding domain that renders it unable to bind specifically to DNA, but maintains the capacity to interact tightly with chromatin. Both the C-terminal domain (CTD) and oligomerization domain (OD) of GOF mtp53 proteins are intact and it is unclear whether these regions of mtp53 are responsible for chromatin-based DNA replication activities. We generated MDA-MB-468 cells with CRISPR-Cas9 edited versions of the CTD and OD regions of mtp53 R273H. These included a frame-shift mtp53 R273H
Volume
12
Issue
12
First Page
1128
Last Page
1146
ISSN
1949-2553
Published In/Presented At
Ellison, V., Annor, G. K., Freedman, C., Xiao, G., Lundine, D., Freulich, E., Prives, C., & Bargonetti, J. (2021). Frame-shift mediated reduction of gain-of-function p53 R273H and deletion of the R273H C-terminus in breast cancer cells result in replication-stress sensitivity. Oncotarget, 12(12), 1128–1146. https://doi.org/10.18632/oncotarget.27975
Disciplines
Medical Education | Medicine and Health Sciences
PubMedID
34136083
Department(s)
USF-LVHN SELECT Program, USF-LVHN SELECT Program Students
Document Type
Article