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Articles by Ke Cong
MRE11 proximal polyadenylation site-mediated looping impacts transcription and genomic stability
Keywords MRE11 DNA replication alternative polyadenylation DNA repair chromatin looping genome stability promoter-3′ UTR looping RNA Pol II recycling transcription Get full text access Log in, subscribe or purchase for full access. References 1. Lal, A. ∙ Pan, Y. ∙ Navarro, F. ... miR-24-mediated downregulation of H2AX suppresses DNA repair in terminally differentiated blood cells Nat. Struct. Mol. Biol. 2009; 16:492-498 2. Moskwa, P. ∙ Buffa, F.M. ∙ Pan, Y. ...
RAD51 is chromatin enriched and targetable in BRCA1-deficient cells
Keywords MDC1 53BP1 H2AX BRCA1 gaps HR PARPi TLS RAD51 foci Introduction Cancer cells deficient in the hereditary breast and ovarian cancer genes, BRCA1 or BRCA2 (BRCA), are hypersensitive to poly (ADP-ribose) polymerase inhibitors (PARPi).
FANCJ promotes PARP1 activity during DNA replication that is essential in BRCA1 deficient cells - Nature Communications
Abstract The effectiveness of poly (ADP-ribose) polymerase inhibitors (PARPi) in creating single-stranded DNA gaps and inducing sensitivity requires the FANCJ DNA helicase. Yet, how FANCJ relates to PARP1 inhibition or trapping, which contribute to PARPi toxicity, remains unclear. Here, we find PARPi effectiveness hinges on S-phase PARP1 activity, which is reduced in FANCJ deficient cells as G-quadruplexes sequester PARP1 and MSH2.
FANCJ promotes PARP1 activity during DNA replication that is essential in BRCA1 deficient cells
Abstract Single-stranded DNA gaps are postulated to be fundamental to the mechanism of anti-cancer drugs. Gaining insights into their induction could therefore be pivotal for advancing therapeutic strategies. For poly (ADP-ribose) polymerase inhibitors (PARPi) to be effective, the presence of FANCJ helicase is required. However, the relationship between FANCJ dependent gaps and PARP1 catalytic inhibition or trapping-both linked to PARPi toxicity in BRCA deficient cells-is yet to be elucidated.
Exploiting replication gaps for cancer therapy
• None The CIP2A-TOPBP1 axis safeguards chromosome stability and is a synthetic lethal target for BRCA-mutated cancer. : • None Ligase 1 is a predictor of platinum resistance and its blockade is synthetically lethal in XRCC1 deficient epithelial ovarian cancers. : • None RNA:DNA hybrids from Okazaki fragment are cis-regulators of Ku function in safeguarding replication fork integrity.
Loss of nuclear DNA ligase III reverts PARP inhibitor resistance in BRCA1/53BP1 double-deficient cells by exposing ssDNA gaps
Arakawa H. Iliakis G. Alternative Okazaki fragment ligation pathway by DNA ligase III. Genes (Basel). 2015; 6: 385-398 Barazas M. Annunziato S. Pettitt S.J. de Krijger I. Ghezraoui H. Roobol S.J. Lutz C. Frankum J. Song F.F. Brough R. et al. The CST complex mediates end protection at double-strand breaks and promotes PARP inhibitor sensitivity in BRCA1-deficient cells. Cell Rep. 2018; 23: 2107-2118 Barazas M. Gasparini A. Huang Y. Küçükosmanoğlu A. Annunziato S. Bouwman P. Sol W. Kersbergen A. Proost N.
Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency
(Molecular Cell 81, 3128–3144.e1–e7; August 5, 2021) In the originally published version of this paper, the order of the author list is incorrect. In the corrected version, which now appears online, the names of John J. Turchi and Jos Jonkers have been switched. The authors regret this error. Article Info Identification DOI: https://doi.org/10.1016/j.molcel.2021.07.015 Copyright © 2021 Elsevier Inc.
Replication gaps are a key determinant of PARP inhibitor synthetic lethality with BRCA deficiency
Adam S. Rossi S.E. Moatti N. Zompit M.D.M. Ng T.F. Álvarez-Quilón A. Desjardins J. Bhaskaran V. Martino G. Setiaputra D. et al. CIP2A is a prime synthetic-lethal target for BRCA-mutated cancers. bioRxiv. 2021; https://doi.org/10.1101/2021.02.08.430060 Álvarez-Quilón A. Wojtaszek J.L. Mathieu M.C. Patel T. Appel C.D. Hustedt N. Rossi S.E. Wallace B.D. Setiaputra D. Adam S. et al. Endogenous DNA 3′ Blocks Are Vulnerabilities for BRCA1 and BRCA2 Deficiency and Are Reversed by the APE2 Nuclease. Mol. Cell.
Replication Gaps Underlie BRCA Deficiency and Therapy Response
Tumor Biology and Immunology Nicholas J. Panzarino, John J. Krais, Ke Cong, Min Peng, Michelle Mosqueda, Sumeet U. Nayak, Samuel M. Bond, Jennifer A. Calvo, Mihir B. Doshi, Matt Bere, Jianhong Ou, Bin Deng, Lihua J. Zhu, Neil Johnson and Sharon B.
Replication Gaps Underlie BRCA-deficiency and Therapy Response
Research Article Nicholas J. Panzarino, John J. Krais, Ke Cong, Min Peng, Michelle Mosqueda, Sumeet U. Nayak, Samuel M. Bond, Jennifer A. Calvo, Mihir B. Doshi, Matt Bere, Jianhong Ou, Bin Deng, Lihua J. Zhu, Neil Johnson and Sharon B. Cantor DOI: 10.1158/0008-5472.CAN-20-1602 Abstract Defects in DNA repair and the protection of stalled DNA replication forks are thought to underlie the chemosensitivity of tumors deficient in the hereditary breast cancer genes BRCA1 and BRCA2 (BRCA).
Replication Gaps Underlie BRCA-deficiency and Therapy Response
Research Article Nicholas J. Panzarino, John J. Krais, Ke Cong, Min Peng, Michelle Mosqueda, Sumeet U. Nayak, Samuel M. Bond, Jennifer A. Calvo, Mihir B. Doshi, Matt Bere, Jianhong Ou, Bin Deng, Lihua J. Zhu, Neil Johnson and Sharon B. Cantor DOI: 10.1158/0008-5472.CAN-20-1602 Abstract Challenging this assumption are recent findings that indicate chemotherapies such as cisplatin used to treat BRCA-deficient tumors do not initially cause DNA double-strand-breaks (DSB).
Inhibition of the translesion synthesis polymerase REV1 exploits replication gaps as a cancer vulnerability
Abstract The replication stress response, which serves as an anticancer barrier, is activated not only by DNA damage and replication obstacles but also oncogenes, thus obscuring how cancer evolves. Here, we identify that oncogene expression, similar to other replication stress–inducing agents, induces single-stranded DNA (ssDNA) gaps that reduce cell fitness.
Opposing Roles of FANCJ and HLTF Protect Forks and Restrain Replication during Stress
The DNA helicase FANCJ is mutated in hereditary breast and ovarian cancer and Fanconi anemia (FA). Nevertheless, how loss of FANCJ translates to disease pathogenesis remains unclear. We addressed this question by analyzing proteins associated with replication forks in cells with or without FANCJ.
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