@article{da386e6a4a0a4d69ab8aef33836e3439,
title = "Chromatin Remodeling and Immediate Early Gene Activation by SLFN11 in Response to Replication Stress",
abstract = "Schlafen 11 (SLFN11), a promising therapeutic biomarker, binds chromatin and sensitizes cancer cells to DNA-targeting agents by blocking DNA replication. Murai et al. show that, in response to replication stress, SLFN11 selectively increases chromatin accessibility at promoters and activates a subset of genes known as the immediate early genes (IEGs).",
keywords = "ATR, CHK1, DNA damage, FOS, JUN, cell cycle checkpoint, chromatin, native immune response, replication stress, topoisomerase inhibitor",
author = "Junko Murai and Hongliang Zhang and Lorinc Pongor and Tang, {Sai Wen} and Ukhyun Jo and Fumiya Moribe and Yixiao Ma and Masaru Tomita and Yves Pommier",
note = "Funding Information: We are grateful to Dr. James Doroshow and the NCI Developmental Therapeutics Program group (DTP-DCTD) for providing the dataset of NCI-60 and drug responses, the CCR sequencing facility for sequencing and analyzing ATAC-seq and ChIP-seq data, and the junior technical assistants (Mr. Kennosuke Sato, Tomohiro Watanabe, and Yui Sato) from Tsuruoka Chuo Senior High School. We also thank the DTP-DCTD, NCI/NIH, for providing the drugs and cell lines used in this study. The study used the high-performance computer capabilities of the Biowulf HPC cluster at the NIH. This project was supported by the Intramural Program, Center for Cancer Research of the National Cancer Institute, NIH (Z01 BC 006161 and 006150) (to Y.P.) and AMED (Japan Agency for Medical Research and Development) Project for Cancer Research and Therapeutic Evolution (to J.M.). Conceptualization, Y.P. and J.M.; Methodology, Y.P. J.M. H.Z. L.P. and S.-w.T.; Software, L.P.; Formal Analysis, J.M. and L.P.; Investigation, J.M. H.Z. L.P. S.-w.T. U.J. F.M. and Y.M.; Writing – Original Draft; J.M. Y.P. and L.P.; Writing – Review & Editing, J.M. Y.P. and L.P.; Visualization, J.M. Y.P. and L.P.; Supervision, Y.P.; Funding Acquisition, Y.P. J.M. and M.T. The authors declare no competing interests. Funding Information: We are grateful to Dr. James Doroshow and the NCI Developmental Therapeutics Program group (DTP-DCTD) for providing the dataset of NCI-60 and drug responses, the CCR sequencing facility for sequencing and analyzing ATAC-seq and ChIP-seq data, and the junior technical assistants (Mr. Kennosuke Sato, Tomohiro Watanabe, and Yui Sato) from Tsuruoka Chuo Senior High School. We also thank the DTP-DCTD, NCI/NIH, for providing the drugs and cell lines used in this study. The study used the high-performance computer capabilities of the Biowulf HPC cluster at the NIH. This project was supported by the Intramural Program, Center for Cancer Research of the National Cancer Institute, NIH ( Z01 BC 006161 and 006150 ) (to Y.P.) and AMED (Japan Agency for Medical Research and Development) Project for Cancer Research and Therapeutic Evolution (to J.M.). Publisher Copyright: {\textcopyright} 2020",
year = "2020",
month = mar,
day = "24",
doi = "10.1016/j.celrep.2020.02.117",
language = "English",
volume = "30",
pages = "4137--4151.e6",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "12",
}
