CtIP mediates replication fork recovery in a FANCD2-regulated manner.

No abstract is available for this paper.

• Publication year

  2014

• Venue

  Human Molecular Genetics

• Publication date

  2014-07-15

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1093/hmg/ddu078PMID 24556218PMCID PMC4065146
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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  2013cited by this paper
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• Involvement of SLX4 in interstrand cross-link repair is regulated by the Fanconi anemia pathway

  2011cited by this paper
• Mutations of the SLX4 gene in Fanconi anemia

  2011cited by this paper
• Mre11 regulates CtIP–dependent double strand break repair by interaction with CDK2

  2011cited by this paper
• BLM has early and late functions in homologous recombination repair in mouse embryonic stem cells

  2010cited by this paper
• Identification of KIAA1018/FAN1, a DNA repair nuclease recruited to DNA damage by monoubiquitinated FANCD2.

  2010cited by this paper
• Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair

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• Susceptibility pathways in Fanconi's anemia and breast cancer.

  2010cited by this paper
• Deficiency of FANCD2-associated nuclease KIAA1018/FAN1 sensitizes cells to interstrand crosslinking agents.

  2010cited by this paper
• A genetic screen identifies FAN1, a Fanconi anemia-associated nuclease necessary for DNA interstrand crosslink repair.

  2010cited by this paper
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  2010cited by this paper
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• Expanded roles of the Fanconi anemia pathway in preserving genomic stability.

  2010cited by this paper
• MRE11–RAD50–NBS1 is a critical regulator of FANCD2 stability and function during DNA double‐strand break repair

  2009cited by this paper
• Bloom DNA Helicase Facilitates Homologous Recombination between Diverged Homologous Sequences*

  2009cited by this paper
• The Fanconi Anemia Protein FANCM Is Controlled by FANCD2 and the ATR/ATM Pathways*

  2009cited by this paper
• PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination

  2009cited by this paper
• MRE11-RAD50-NBS1 Complex Dictates DNA Repair Independent of H2AX*

  2009cited by this paper
• Expression of PCNA-binding domain of CtIP, a motif required for CtIP localization at DNA replication foci, causes DNA damage and activation of DNA damage checkpoint

  2009cited by this paper
• FANCG promotes formation of a newly identified protein complex containing BRCA2, FANCD2 and XRCC3

  2008cited by this paper
• RMI, a new OB-fold complex essential for Bloom syndrome protein to maintain genome stability.

  2008cited by this paper
• Cell Cycle-dependent Complex Formation of BRCA1·CtIP·MRN Is Important for DNA Double-strand Break Repair*

  2008cited by this paper
• Human CtIP promotes DNA end resection

  2007cited by this paper
• ATM and the Mre11 complex combine to recognize and signal DNA double-strand breaks

  2007cited by this paper
• Identification of the FANCI protein, a monoubiquitinated FANCD2 paralog required for DNA repair.

  2007cited by this paper
• Role for BLM in replication-fork restart and suppression of origin firing after replicative stress

  2007cited by this paper
• Emergence of a DNA-damage response network consisting of Fanconi anaemia and BRCA proteins

  2007cited by this paper
• Dormant origins licensed by excess Mcm2-7 are required for human cells to survive replicative stress.

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• BRCA1 ubiquitinates its phosphorylation-dependent binding partner CtIP.

  2006cited by this paper
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• Homology-directed dna repair, mitomycin-c resistance, and chromosome stability is restored with correction of a Brca1 mutation.

  2001cited by this paper
• Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway.

  2001cited by this paper
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  2000cited by this paper
• Independence of R/M/N focus formation and the presence of intact BRCA1.

  2000cited by this paper
• Nuclear Localization and Cell Cycle-specific Expression of CtIP, a Protein That Associates with the BRCA1 Tumor Suppressor*

  2000cited by this paper
• Interaction between a Cellular Protein That Binds to the C-terminal Region of Adenovirus E1A (CtBP) and a Novel Cellular Protein Is Disrupted by E1A through a Conserved PLDLS Motif*

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  1998cited by this paper
• Association of BRCA1 with Rad51 in mitotic and meiotic cells.

  1997cited by this paper
• Edinburgh Research Explorer Disruption of mouse Slx4, a regulator of structure-specific nucleases, phenocopies Fanconi anemia

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  2025cites this paper
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  2025cites this paper
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  2025cites this paper
• FANCD2 counteracts O6-methylguanine-induced mismatch repair-dependent apoptosis

  2024cites this paper
• Replication stress as a driver of cellular senescence and aging

  2024cites this paper
• The Fanconi anemia core complex promotes CtIP-dependent end-resection to drive homologous recombination at DNA double-strand breaks

  2023cites this paper
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  2023cites this paper
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  2022cites this paper
• RNAi Screening Uncovers a Synthetic Sick Interaction between CtIP and the BARD1 Tumor Suppressor

  2022cites this paper
• SIAH2 regulates DNA end resection and replication fork recovery by promoting CtIP ubiquitination

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• CST in maintaining genome stability: Beyond telomeres.

  2021cites this paper
• FANCD2 and RAD51 recombinase directly inhibit DNA2 nuclease at stalled replication forks and FANCD2 acts as a novel RAD51 mediator in strand exchange to promote genome stability

  2021influential citation
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