Lise M van Wijk, Andreea B Nilas, Harry Vrieling, Maaike P G Vreeswijk. Expert Rev Mol Diagn 2022
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ATR-Mediated Global Fork Slowing and Reversal Assist Fork Traverse and Prevent Chromosomal Breakage at DNA Interstrand Cross-Links.
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Genetic Screens Reveal FEN1 and APEX2 as BRCA2 Synthetic Lethal Targets.
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Resistance to therapy in BRCA2 mutant cells due to loss of the nucleosome remodeling factor CHD4.
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The CIP2A-TOPBP1 axis safeguards chromosome stability and is a synthetic lethal target for BRCA-mutated cancer.
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Inhibition of the translesion synthesis polymerase REV1 exploits replication gaps as a cancer vulnerability.
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HPF1-dependent PARP activation promotes LIG3-XRCC1-mediated backup pathway of Okazaki fragment ligation.
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Identification of Small Molecule Translesion Synthesis Inhibitors That Target the Rev1-CT/RIR Protein-Protein Interaction.
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A distinct replication fork protection pathway connects Fanconi anemia tumor suppressors to RAD51-BRCA1/2.
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Replication Gaps Underlie BRCA Deficiency and Therapy Response.
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Poly(ADP-ribose) polymerase is hyperactivated in homologous recombination-defective cells.
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53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks.
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PARP inhibition impedes the maturation of nascent DNA strands during DNA replication.
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BRCA2 associates with MCM10 to suppress PRIMPOL-mediated repriming and single-stranded gap formation after DNA damage.
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Loss of nuclear DNA ligase III reverts PARP inhibitor resistance in BRCA1/53BP1 double-deficient cells by exposing ssDNA gaps.
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Trapping of PARP1 and PARP2 by Clinical PARP Inhibitors.
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Rad52 inactivation is synthetically lethal with BRCA2 deficiency.
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Revisiting the BRCA-pathway through the lens of replication gap suppression: "Gaps determine therapy response in BRCA mutant cancer".
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Restored replication fork stabilization, a mechanism of PARP inhibitor resistance, can be overcome by cell cycle checkpoint inhibition.
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Temporally distinct post-replicative repair mechanisms fill PRIMPOL-dependent ssDNA gaps in human cells.
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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.