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Molecular Cell|October 4, 2011
BRCA1 is required for postreplication repair after UV-induced DNA damageShailja Pathania, Jenna Nguyen, Sarah J Hill, et al.
Molecular Cell|August 18, 2009
Cdk1 participates in BRCA1-dependent S phase checkpoint control in response to DNA damageNeil Johnson, Dongpo Cai, Richard D Kennedy, et al.
Molecular Cell|July 5, 2016
BRCA1/FANCD2/BRG1-Driven DNA Repair Stabilizes the Differentiation State of Human Mammary Epithelial CellsHua Wang, Brian Bierie, Andrew G Li, et al.
The Journal of Cell Biology|May 12, 2020
E3 ligase RFWD3 is a novel modulator of stalled fork stability in BRCA2-deficient cellsHaohui Duan, Sarah Mansour, Rachel Reed, et al.
Cell Reports|September 20, 2023
Replication stress and defective checkpoints make fallopian tube epithelial cells putative drivers of high-grade serous ovarian cancerPamoda Galhenage, Yunlan Zhou, Erica Perry, et al.
Proceedings of the National Academy of Sciences of the United States of America|July 1, 2020
Fibroblast-tumor cell signaling limits HER2 kinase therapy response via activation of MTOR and antiapoptotic pathwaysIoannis K Zervantonakis, Matthew D Poskus, Alexis L Scott, et al.
Nature Communications|November 18, 2014
BRCA1 haploinsufficiency for replication stress suppression in primary cellsShailja Pathania, Sangeeta Bade, Morwenna Le Guillou, et al.
Molecular Cell|February 21, 2015
BRCA1 recruitment to transcriptional pause sites is required for R-loop-driven DNA damage repairElodie Hatchi, Konstantina Skourti-Stathaki, Steffen Ventz, et al.
Cancer Discovery|February 3, 2019
MAPK Pathway Suppression Unmasks Latent DNA Repair Defects and Confers a Chemical Synthetic Vulnerability in <i>BRAF-, NRAS</i>-, and <i>NF1</i>-Mutant MelanomasOphélia Maertens, Ryan Kuzmickas, Haley E Manchester, et al.
Proceedings of the National Academy of Sciences of the United States of America|October 5, 2021
<i>BRCA1/Trp53</i> heterozygosity and replication stress drive esophageal cancer development in a mouse modelYe He, Joshua Rivera, Miklos Diossy, et al.
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