Weiran Feng, Maria Jasin. Nat Commun 2017
Times Cited: 82
Times Cited: 82
Times Cited
Times Co-cited
Similarity
Double-strand break repair-independent role for BRCA2 in blocking stalled replication fork degradation by MRE11.
Katharina Schlacher, Nicole Christ, Nicolas Siaud, Akinori Egashira, Hong Wu, Maria Jasin. Cell 2011
Katharina Schlacher, Nicole Christ, Nicolas Siaud, Akinori Egashira, Hong Wu, Maria Jasin. Cell 2011
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Replication fork stability confers chemoresistance in BRCA-deficient cells.
Arnab Ray Chaudhuri, Elsa Callen, Xia Ding, Ewa Gogola, Alexandra A Duarte, Ji-Eun Lee, Nancy Wong, Vanessa Lafarga, Jennifer A Calvo, Nicholas J Panzarino,[...]. Nature 2016
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A distinct replication fork protection pathway connects Fanconi anemia tumor suppressors to RAD51-BRCA1/2.
Katharina Schlacher, Hong Wu, Maria Jasin. Cancer Cell 2012
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Replication fork reversal triggers fork degradation in BRCA2-defective cells.
Sofija Mijic, Ralph Zellweger, Nagaraja Chappidi, Matteo Berti, Kurt Jacobs, Karun Mutreja, Sebastian Ursich, Arnab Ray Chaudhuri, Andre Nussenzweig, Pavel Janscak,[...]. Nat Commun 2017
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Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells.
Ralph Zellweger, Damian Dalcher, Karun Mutreja, Matteo Berti, Jonas A Schmid, Raquel Herrador, Alessandro Vindigni, Massimo Lopes. J Cell Biol 2015
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MRE11 and EXO1 nucleases degrade reversed forks and elicit MUS81-dependent fork rescue in BRCA2-deficient cells.
Delphine Lemaçon, Jessica Jackson, Annabel Quinet, Joshua R Brickner, Shan Li, Stephanie Yazinski, Zhongsheng You, Grzegorz Ira, Lee Zou, Nima Mosammaparast,[...]. Nat Commun 2017
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Smarcal1-Mediated Fork Reversal Triggers Mre11-Dependent Degradation of Nascent DNA in the Absence of Brca2 and Stable Rad51 Nucleofilaments.
Arun Mouli Kolinjivadi, Vincenzo Sannino, Anna De Antoni, Karina Zadorozhny, Mairi Kilkenny, Hervé Técher, Giorgio Baldi, Rong Shen, Alberto Ciccia, Luca Pellegrini,[...]. Mol Cell 2017
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Rad51 protects nascent DNA from Mre11-dependent degradation and promotes continuous DNA synthesis.
Yoshitami Hashimoto, Arnab Ray Chaudhuri, Massimo Lopes, Vincenzo Costanzo. Nat Struct Mol Biol 2010
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Restoration of Replication Fork Stability in BRCA1- and BRCA2-Deficient Cells by Inactivation of SNF2-Family Fork Remodelers.
Angelo Taglialatela, Silvia Alvarez, Giuseppe Leuzzi, Vincenzo Sannino, Lepakshi Ranjha, Jen-Wei Huang, Chioma Madubata, Roopesh Anand, Brynn Levy, Raul Rabadan,[...]. Mol Cell 2017
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Synthetic viability by BRCA2 and PARP1/ARTD1 deficiencies.
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EZH2 promotes degradation of stalled replication forks by recruiting MUS81 through histone H3 trimethylation.
Beatrice Rondinelli, Ewa Gogola, Hatice Yücel, Alexandra A Duarte, Marieke van de Ven, Roxanne van der Sluijs, Panagiotis A Konstantinopoulos, Jos Jonkers, Raphaël Ceccaldi, Sven Rottenberg,[...]. Nat Cell Biol 2017
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MUS81 nuclease activity is essential for replication stress tolerance and chromosome segregation in BRCA2-deficient cells.
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DNA2 drives processing and restart of reversed replication forks in human cells.
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53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks.
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Replication fork reversal in eukaryotes: from dead end to dynamic response.
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Replication stress activates DNA repair synthesis in mitosis.
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Human RECQ1 promotes restart of replication forks reversed by DNA topoisomerase I inhibition.
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ATR phosphorylates SMARCAL1 to prevent replication fork collapse.
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Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase.
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Hydroxyurea-stalled replication forks become progressively inactivated and require two different RAD51-mediated pathways for restart and repair.
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53BP1 nuclear bodies form around DNA lesions generated by mitotic transmission of chromosomes under replication stress.
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Mammalian RAD51 paralogs protect nascent DNA at stalled forks and mediate replication restart.
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RADX Promotes Genome Stability and Modulates Chemosensitivity by Regulating RAD51 at Replication Forks.
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ATR inhibition disrupts rewired homologous recombination and fork protection pathways in PARP inhibitor-resistant BRCA-deficient cancer cells.
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Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy.
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Causes and consequences of replication stress.
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A Dominant Mutation in Human RAD51 Reveals Its Function in DNA Interstrand Crosslink Repair Independent of Homologous Recombination.
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Topoisomerase I poisoning results in PARP-mediated replication fork reversal.
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Replication Fork Slowing and Reversal upon DNA Damage Require PCNA Polyubiquitination and ZRANB3 DNA Translocase Activity.
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Homologous recombination and human health: the roles of BRCA1, BRCA2, and associated proteins.
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Resistance to therapy in BRCA2 mutant cells due to loss of the nucleosome remodeling factor CHD4.
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Fanconi-Anemia-Associated Mutations Destabilize RAD51 Filaments and Impair Replication Fork Protection.
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HLTF's Ancient HIRAN Domain Binds 3' DNA Ends to Drive Replication Fork Reversal.
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Purified human BRCA2 stimulates RAD51-mediated recombination.
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Polyubiquitinated PCNA recruits the ZRANB3 translocase to maintain genomic integrity after replication stress.
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SMARCAL1 catalyzes fork regression and Holliday junction migration to maintain genome stability during DNA replication.
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Replication Fork Reversal: Players and Guardians.
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ATR prohibits replication catastrophe by preventing global exhaustion of RPA.
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Mammalian RAD52 Functions in Break-Induced Replication Repair of Collapsed DNA Replication Forks.
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BOD1L Is Required to Suppress Deleterious Resection of Stressed Replication Forks.
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Mammalian polymerase θ promotes alternative NHEJ and suppresses recombination.
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Moonlighting at replication forks - a new life for homologous recombination proteins BRCA1, BRCA2 and RAD51.
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Co-cited is the co-citation frequency, indicating how many articles cite the article together with the query article. Similarity is the co-citation as percentage of the times cited of the query article or the article in the search results, whichever is the lowest. These numbers are calculated for the last 100 citations when articles are cited more than 100 times.