Protein Degradation Pathways Regulate the Functions of Helicases in the DNA Damage Response and Maintenance of Genomic Stability (original) (raw)

Preventing over-resection by DNA2 helicase/nuclease suppresses repair defects in Fanconi anemia cells

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A minimal threshold of FANCJ helicase activity is required for its response to replication stress or double-strand break repair

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Ubiquitin-dependent recruitment of the Bloom Syndrome helicase upon replication stress is required to suppress homologous recombination

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FANCJ (BACH1) helicase forms DNA damage inducible foci with replication protein A and interacts physically and functionally with the single-stranded DNA-binding protein

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FANCJ DNA helicase is recruited to the replisome by AND-1 to ensure genome stability

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BLM and the FANC proteins collaborate in a common pathway in response to stalled replication forks

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How Fanconi anemia proteins promote the four Rs: Replication, recombination, repair, and recovery

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Bloom's Syndrome Helicase and Mus81 are Required to Induce Transient Double-strand DNA Breaks in Response to DNA Replication Stress

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The human F-Box DNA helicase FBH1 faces Saccharomyces cerevisiae Srs2 and postreplication repair pathway roles

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Mitotic phosphorylation of Bloom helicase at Thr182 is required for its proteasomal degradation and maintenance of chromosomal stability

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Werner Syndrome Helicase Has a Critical Role in DNA Damage Responses in the Absence of a Functional Fanconi Anemia Pathway

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Homology-directed Fanconi anemia pathway cross-link repair is dependent on DNA replication

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Central Role of Ubiquitination in Genome Maintenance: DNA Replication and Damage Repair

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Cell Cycle-dependent Regulation of a Human DNA Helicase That Localizes in DNA Damage Foci

Jinming Gu

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Posttranslational modifications of repair factors and histones in the cellular response to stalled replication forks

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FANCJ helicase promotes DNA end resection by facilitating CtIP recruitment to DNA double-strand breaks

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The Fanconi anemia pathway and the DNA interstrand cross-links repair

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Fanconi Anemia Proteins and the S Phase Checkpoint

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A Role for the Fanconi Anemia C Protein in Maintaining the DNA Damage-induced G2 Checkpoint

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RecQ-like helicases: the DNA replication checkpoint connection

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14-3-3 checkpoint regulatory proteins interact specifically with DNA repair protein human exonuclease 1 (hEXO1) via a semi-conserved motif

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MRN complex-dependent recruitment of ubiquitylated BLM helicase to DSBs negatively regulates DNA repair pathways

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Human Fanconi anemia monoubiquitination pathway promotes homologous DNA repair

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FANCM regulates repair pathway choice at stalled replication forks

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The helicase FBH1 is tightly regulated by PCNA via CRL4(Cdt2)-mediated proteolysis in human cells

Bernard Lopez

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Ubiquitinated Fancd2 recruits Fan1 to stalled replication forks to prevent genome instability

Julian Blow

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DNA2 and EXO1 in replication-coupled, homology-directed repair and in the interplay between HDR and the FA/BRCA network

Kenneth Karanja

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The Fanconi anaemia components UBE2T and FANCM are functionally linked to nucleotide excision repair

Arno Alpi

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BLM helicase–dependent and –independent roles of 53BP1 during replication stress–mediated homologous recombination

Vivek Tripathi

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The mismatch DNA repair heterodimer, hMSH2/6, regulates BLM helicase

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FBH1 promotes DNA double-strand breakage and apoptosis in response to DNA replication stress

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Recruitment of Fanconi Anemia and Breast Cancer Proteins to DNA Damage Sites Is Differentially Governed by Replication

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The ubiquitous role of ubiquitin in the DNA damage response

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The role of the Fanconi anemia network in the response to DNA replication stress

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