Affinage

POLE3

DNA polymerase epsilon subunit 3 · UniProt Q9NRF9

Length
147 aa
Mass
16.9 kDa
Annotated
2026-06-10
37 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

POLE3 (CHRAC17/Dpb4/YBL1) is a histone-fold accessory subunit of leading-strand DNA polymerase epsilon that doubles as a histone H3-H4 chaperone coordinating DNA replication with chromatin assembly (PMID:30217558, PMID:11000277). As a POLE3-POLE4 subcomplex, it selectively binds histones H3-H4, promotes tetrasome formation and DNA supercoiling in vitro, binds both parental and newly synthesized histones, and is required for coordinated parental histone retention and new histone deposition at the replication fork (PMID:30217558); together with Mcm2 and POLE4 it mediates transfer of parental H3.1 and H3.3, and loss of this activity causes chromosome segregation defects (PMID:35523900). By enforcing symmetric parental histone deposition, POLE3 sustains faithful epigenetic inheritance: its deletion in embryonic stem cells distorts H3.3 and H3K27me3 patterning at developmental loci and impairs neural differentiation (PMID:37666989). POLE3-POLE4 also enhances Polε processivity, with POLE4 deficiency destabilizing the polymerase complex and causing replication stress and inefficient origin firing (PMID:29754823), and it 'grips' newly synthesized dsDNA on the leading strand in parallel with CHTF18-RFC2/5-mediated PCNA loading, the two pathways being synthetically lethal when combined (PMID:41339636). Through its histone-fold domain, POLE3 heterodimerizes with CHRAC15/CHRAC1 in the CHRAC complex (ACF1-SNF2H) to facilitate ATP-dependent nucleosome sliding and chromatin assembly (PMID:14759371), and this complex promotes both NHEJ and HR repair of double-strand breaks downstream of KU recruitment (PMID:21172662, PMID:37682991). Via Polε it links to the HUSH complex to drive asymmetric H3K9me3 segregation onto leading strands at LINE retrotransposons, silencing their expression (PMID:37938774), and it maintains repressive chromatin on unintegrated HIV-1 DNA by blocking RNAPII recruitment (PMID:37922361). Loss of POLE3-POLE4 sensitizes cancer cells to PARP inhibitors independently of homologous recombination, instead triggering PRIMPOL-dependent replicative single-stranded gap accumulation (PMID:38753485, PMID:38828775).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2000 Medium

    Established POLE3 as a histone-fold protein capable of forming histone-containing nucleosomal complexes, framing it as a chromatin-associated factor rather than a sequence-specific transcription factor.

    Evidence Nucleosome reconstitution, glycerol gradient sedimentation and DNA binding assays of YBL1/POLE3

    PMID:11000277

    Open questions at the time
    • Did not define the in vivo complexes or partners
    • No replication-fork or repair function assigned
  2. 2004 High

    Resolved two distinct complex contexts for the POLE3 histone-fold, showing it heterodimerizes with CHRAC15 to enhance ACF nucleosome sliding/assembly and separately pairs with POLE4 in Polε.

    Evidence Biochemical reconstitution of nucleosome sliding and chromatin assembly with interaction mapping

    PMID:14759371

    Open questions at the time
    • In vivo significance of each complex not tested
    • No link to DNA repair or replication phenotypes yet
  3. 2006 Medium

    Defined cell-cycle-coupled transcriptional control of POLE3, consistent with an S-phase replication role.

    Evidence Promoter mutagenesis, reporter clones and ChIP for E2F1/4 and MYC

    PMID:16403426

    Open questions at the time
    • Regulation of protein function during the cycle not addressed
    • No connection to the encoded protein's activity
  4. 2008 Medium

    Placed POLE3/POLE4 within human ATAC acetyltransferase complexes, broadening its connection between chromatin remodeling and transcriptional regulation.

    Evidence Biochemical purification and mass spectrometry of ATAC complex

    PMID:18838386

    Open questions at the time
    • No POLE3-specific mutagenesis within ATAC
    • Functional contribution of POLE3 to ATAC activity untested
  5. 2011 High

    Showed the CHRAC complex containing POLE3 acts in DNA double-strand break repair, extending its remodeling role to genome maintenance.

    Evidence Co-IP of chromatin association after DSBs, siRNA with NHEJ/HR reporters and X-ray sensitivity

    PMID:21172662

    Open questions at the time
    • Mechanism of chromatin recruitment to breaks unclear
    • Did not separate CHRAC vs Polε contributions
  6. 2018 High

    Defined POLE3-POLE4 as a histone H3-H4 chaperone subcomplex of Polε that couples histone deposition to the replication fork and supports Polε processivity, establishing the core replication-coupled chromatin function.

    Evidence HDX-MS, in vitro tetrasome/supercoiling assays, chromatin fractionation; Pole4 KO mouse with replication-stress and origin-firing readouts and p53 rescue

    PMID:29754823 PMID:30217558

    Open questions at the time
    • Strand asymmetry of histone partitioning not yet resolved
    • Yeast orthologs dispensable for viability, raising species-specific essentiality questions
  7. 2021 High

    Demonstrated via the yeast ortholog that the POLE3 histone-fold operates in two complexes at DSBs—promoting resection in ISW2 and checkpoint activation in Polε—mapping a domain-level basis for its repair roles.

    Evidence Genetic epistasis, ChIP, resection and checkpoint assays with histone-fold mutagenesis in S. cerevisiae

    PMID:34362907

    Open questions at the time
    • Direct human orthology of these specific activities not shown
    • Structural basis of partner selection unresolved
  8. 2022 High

    Established POLE3 as part of the parental-histone transfer machinery with Mcm2 and POLE4, linking faithful histone inheritance to accurate chromosome segregation, and revealed a parallel leading-strand replication pathway with DSCC1-RFC.

    Evidence SNAP-tag pulse-chase histone tracking with segregation assays; CRISPR screen and DNA fiber analysis of DSCC1-POLE3 synthetic lethality

    PMID:35523900 PMID:36622344

    Open questions at the time
    • Strand bias of transfer not fully defined
    • Molecular geometry of the Mcm2-POLE3-POLE4 transfer unknown
  9. 2023 High

    Connected POLE3-mediated symmetric histone deposition to epigenetic inheritance and development, and uncovered roles in directing H3K9me3 asymmetry at LINEs and silencing unintegrated HIV-1 DNA, plus a CHRAC1-dependent DSB repair function.

    Evidence Pole3 KO ESCs with ChIP-seq and differentiation assays; HUSH Co-IP, KO cells and strand-specific H3K9me3; RNAPII ChIP and HIV integration assays; POLE3-CHRAC1 Co-IP with KU80 recruitment

    PMID:37666989 PMID:37682991 PMID:37922361 PMID:37938774

    Open questions at the time
    • How leading-strand bias is converted into stable epigenetic asymmetry mechanistically unresolved
    • CHRAC1 interaction lacks structural validation
  10. 2024 High

    Identified POLE3-POLE4 loss as an HR-independent vulnerability to PARP inhibitors driven by PRIMPOL-dependent replicative gap accumulation, defining a distinct synthetic-lethality mechanism.

    Evidence CRISPR KO with RAD51 foci, ssDNA gap detection, PRIMPOL and 53BP1 epistasis, DNA fiber and ATR/DNA-PK signaling readouts

    PMID:38753485 PMID:38828775

    Open questions at the time
    • Direct biochemical cause of gap formation in POLE3-POLE4 deficiency not isolated
    • Translational thresholds for therapeutic exploitation undefined
  11. 2025 High

    Mechanistically separated POLE3-POLE4's leading-strand dsDNA 'gripping' from CHTF18-RFC PCNA loading and identified covalent and ubiquitin-regulatory control points on POLE3.

    Evidence CRISPR screens, structural modelling and biochemistry for processivity; covalent Cys51 modification by MS/competitive pulldown; USP15 Co-IP and ubiquitination assays

    PMID:41164343 PMID:41339636 PMID:41950365

    Open questions at the time
    • Atomic structure of the DNA-gripping interaction not solved
    • USP15 regulation and covalent targeting characterized in single labs only

Open questions

Synthesis pass · forward-looking unresolved questions
  • How POLE3 mechanistically selects and partitions parental histones to specific strands and integrates its replication, repair, and silencing functions into a unified molecular geometry remains unresolved.
  • No high-resolution structure of POLE3 within Polε bound to histones and DNA
  • Determinants partitioning POLE3 among Polε, CHRAC, ATAC and ISW2 contexts undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0042393 histone binding 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0003677 DNA binding 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 2
Pathway
R-HSA-4839726 Chromatin organization 3 R-HSA-69306 DNA Replication 3 R-HSA-73894 DNA Repair 3 R-HSA-1640170 Cell Cycle 2
Partners
ACF1CHRAC1MCM2MPP8POLE4SNF2HTASORUSP15
Complex memberships
ATACCHRAC (ACF1-SNF2H-CHRAC15-CHRAC17)DNA polymerase epsilonISW2 (yeast ortholog)

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 POLE3-POLE4 forms a histone H3-H4 chaperone subcomplex of DNA polymerase epsilon that selectively binds histones H3-H4, promotes tetrasome formation and DNA supercoiling in vitro, and in cells binds both newly synthesized and parental histones; its depletion hinders helicase unwinding, chromatin PCNA unloading, and compromises coordinated parental histone retention and new histone deposition at the replication fork. Hydrogen/deuterium exchange mass spectrometry, physical domain mapping, in vitro tetrasome formation and DNA supercoiling assays, cellular depletion with chromatin fractionation and PCNA unloading readouts Molecular cell High 30217558
2018 POLE4 deficiency in mice destabilizes the entire Polε complex (including POLE3), leading to replication stress and inefficient replication origin firing, attributable to the role of POLE3/POLE4 in promoting Polε processivity; budding yeast orthologs of POLE3/POLE4 promote Polε processivity in vitro but are dispensable for viability in vivo. Pole4 knockout mouse model, replication stress markers (p53 activation), origin firing assays, genetic rescue by p53 removal, comparison to yeast in vitro processivity data Molecular cell High 29754823
2004 CHRAC-17 (POLE3) heterodimerizes with CHRAC-15 via histone-fold domains; the CHRAC-15/17 dimer directly interacts with ACF1 and facilitates ATP-dependent nucleosome sliding by ACF. CHRAC-15 is essential for interaction with ACF and sliding enhancement. CHRAC-17 also interacts with p12 (POLE4) in DNA polymerase epsilon. Additionally, the CHRAC-15/17 and p12/CHRAC-17 complexes facilitate ACF-mediated chromatin assembly by a mechanism distinct from nucleosome sliding. Biochemical reconstitution of nucleosome sliding assays, direct interaction mapping, chromatin assembly assays Molecular cell High 14759371
2010 CHRAC17 (POLE3) is a component of the CHRAC complex (ACF1-SNF2H-CHRAC15-CHRAC17) that becomes more associated with chromatin after DSBs; the CHRAC complex is required for both NHEJ and HR repair of DSBs in human cells, acting downstream of KU70/80 recruitment. Co-IP/co-immunoprecipitation showing increased CHRAC complex-chromatin association after DSBs, siRNA knockdown with DSB repair frequency assays (NHEJ and HR reporters), X-ray sensitivity assays Molecular cell High 21172662
2008 POLE3 (CHRAC17) and POLE4 are components of human ATAC-type complexes containing GCN5/PCAF acetyltransferases, linking chromatin assembly/remodeling and DNA replication machineries to histone acetylation and transcriptional regulation. Biochemical purification and characterization of human ATAC complex; mass spectrometry identification of components The Journal of biological chemistry Medium 18838386
2021 Budding yeast Dpb4 (ortholog of POLE3/CHRAC17) acts in two distinct protein complexes at DNA double-strand breaks: (1) interacting with Dls1 in the ISW2 complex to facilitate Isw2 ATPase association and promote histone removal/DSB resection; and (2) interacting with Dpb3 in the Pol ε complex to facilitate Rad9 checkpoint protein association at DSBs and promote checkpoint activation. A Dpb4 A62S histone fold domain mutation enhances these activities. Genetic epistasis, chromatin immunoprecipitation, double mutant analysis in S. cerevisiae, checkpoint activation assays, DSB resection assays Nature communications High 34362907
2023 POLE3-POLE4 interact with the HUSH complex (MPP8 and TASOR) via the leading-strand polymerase Pol ε and contribute to asymmetric segregation of H3K9me3 preferentially onto leading strands at LINE retrotransposons; cells deficient in POLE3 and POLE4 show compromised H3K9me3 asymmetry and increased LINE expression. Co-immunoprecipitation, POLE3/POLE4 knockout cells, ChIP-seq/strand-specific H3K9me3 analysis, MPP8 mutant defective in H3K9me3 binding, TASOR mutants with reduced Pol ε interaction Nature High 37938774
2022 Pole3 (together with Mcm2 and Pole4) mediates transfer of both parental H3.1 and H3.3 histones following DNA replication; Mcm2, Pole3, and Pole4 mutants defective in parental histone transfer show defects in chromosome segregation. SNAP-tag pulse-chase for parental histone tracking, mutant cell lines, chromosome segregation assays Nature communications High 35523900
2023 Pole3 deletion in mouse embryonic stem cells causes aberrant histone landscapes (altered H3.3 and H3K27me3 patterning at differentiation gene regulatory sites) and impaired neural differentiation, demonstrating that symmetric parental histone deposition mediated by Pole3 is required for faithful epigenetic inheritance and developmental gene regulation. Pole3 knockout ESCs, ChIP-seq for H3.3 and H3K27me3, neural differentiation assays, comparison with Mcm2 histone-binding mutants Nature genetics High 37666989
2023 POLE3 interacts with CHRAC1 (CHRAC15) to promote DNA double-strand break repair by regulating expression of homology-directed repair proteins and KU80 recruitment; a CHRAC1 D121Y cancer mutation attenuates the POLE3-CHRAC1 interaction and impairs DNA repair. Co-immunoprecipitation, siRNA knockdown, KU80 recruitment assays, HDR protein expression analysis, cancer mutation analysis Science advances Medium 37682991
2023 POLE3 maintains unintegrated HIV-1 DNA in a repressive chromatin state by preventing RNAPII recruitment to the viral promoter. Loss of POLE3 reduces HIV-1 integration efficiency and impairs viral replication, revealing POLE3 as a repressor of unintegrated retroviral DNA. siRNA knockdown and CRISPR knockout of POLE3, chromatin immunoprecipitation for RNAPII, HIV-1 integration efficiency assays, innate immune sensing assays in primary CD4+ T cells Science advances Medium 37922361
2020 The histone fold domain of POLE3 has a stage-specific function during T and B cell development; mice with viable hypomorphic and neomorphic Pole3 alleles display tissue-restricted lymphocyte developmental defects. Progressive introduction of positively charged residues into the acidic C terminus causes peripheral lymphopenia of increasing severity, indicating the acidic C terminus is functionally important for lymphocyte homeostasis. Pole3 knockout and hypomorphic/neomorphic allele mice, flow cytometry of lymphocyte populations, genetic allelic series with targeted C-terminal charge mutations Cell reports Medium 32553171
2024 Loss of POLE3-POLE4 sensitizes cancer cells to PARP inhibitors in a manner independent of homologous recombination deficiency; PARPi treatment triggers replicative gap accumulation in POLE3-POLE4 KO cells in a PRIMPOL-dependent manner. Knockdown of 53BP1 does not rescue PARPi sensitivity in POLE3-POLE4 KO cells, distinguishing this mechanism from common PARPi resistance pathways. CRISPR knockout of POLE3-POLE4, RAD51 foci formation assays, ssDNA gap accumulation assays, PRIMPOL dependency experiments, 53BP1 knockdown epistasis, BRCA1-silenced cell combination studies Cell reports High 38753485
2024 Loss of POLE4 (and POLE3) sensitizes cells to PARP inhibitors via impaired post-replicative repair leading to single-stranded DNA gap accumulation behind replication forks, with elevated ATR and DNA-PK replication stress signaling; this mechanism acts in parallel to BRCA1 and can counteract acquired PARPi resistance. POLE4 knockout cells, DNA fiber assays (replication speed), ssDNA gap detection, ATR/DNA-PK phosphorylation readouts, BRCA1 epistasis experiments, PARPi sensitivity assays Nucleic acids research High 38828775
2025 POLE3-POLE4 'grips' newly synthesized dsDNA at the replication fork to promote Polε processivity on the leading strand; this function is distinct from and works in parallel with leading strand-specific PCNA loading by CHTF18-RFC2/5. Combined loss of POLE3-POLE4 and CHTF18-RFC2/5 is synthetically lethal and incompatible with leading strand synthesis. Iron metabolism genes are required to sustain Iron-Sulphur Cluster-dependent Polε activity. CRISPR genetic screens in POLE4-deficient cells, structural modelling, biochemistry, cell biology assays for leading strand synthesis and PCNA loading Nature communications High 41339636
2000 YBL1 (POLE3) belongs to the H2A-H2B sub-family of histone fold proteins related to NF-YB and NC2; it forms complexes with histones in solution and on DNA in nucleosome reconstitution assays, and is part of relatively large complexes by glycerol gradient sedimentation, but lacks intrinsic CCAAT- or TATA-binding capacity. Nucleosome reconstitution assays, glycerol gradient sedimentation, DNA binding assays Nucleic acids research Medium 11000277
2006 The Pole3 promoter is bidirectional, lacks CCAAT and TATA boxes, and is regulated in a cell-cycle-dependent manner (peaking at S phase entry). E2F1/4 and MYC bind the Pole3 promoter in a phase-specific manner as shown by chromatin immunoprecipitation; an E-box and neighbouring direct repeat are important for regulation. Promoter mutagenesis, stable reporter clones, chromatin immunoprecipitation for E2F1/4 and MYC Gene Medium 16403426
2026 USP15 binds POLE3 (confirmed by Co-IP) and suppresses its ubiquitination-dependent degradation, thereby stabilizing POLE3 and facilitating DNA damage repair and cisplatin resistance in pancreatic cancer cells. Co-immunoprecipitation, ubiquitination assays, loss-of-function and gain-of-function studies, xenograft model, neutral comet assays Molecular carcinogenesis Medium 41950365
2025 POLE3 is covalently modified at Cys51 by alkaloidal Michael acceptor compound 15, and this covalent targeting of POLE3 identified via competitive pull-down and mass spectrometry contributes to anti-HBV activity (reducing cccDNA and rcDNA levels). Competitive pull-down with biotin/fluorescent-tagged probe, mass spectrometry identification of Cys51 modification, POLE3 knockdown functional validation RSC chemical biology Medium 41164343
2022 DSCC1 and POLE3 show a synthetic lethal interaction; co-depletion of DSCC1 and POLE3 (both interacting with the catalytic Polε subunit) additively impairs DNA replication, suggesting DSCC1-RFC and POLE3 contribute to leading-strand DNA replication in parallel pathways. Genome-wide CRISPR screens in DSCC1-KO cells, co-depletion replication assays, DNA fiber analysis Life science alliance Medium 36622344

Source papers

Stage 0 corpus · 37 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 Human ATAC Is a GCN5/PCAF-containing acetylase complex with a novel NC2-like histone fold module that interacts with the TATA-binding protein. The Journal of biological chemistry 176 18838386
2010 The ACF1 complex is required for DNA double-strand break repair in human cells. Molecular cell 171 21172662
2015 Frequency and phenotypic spectrum of germline mutations in POLE and seven other polymerase genes in 266 patients with colorectal adenomas and carcinomas. International journal of cancer 119 25529843
2018 POLE3-POLE4 Is a Histone H3-H4 Chaperone that Maintains Chromatin Integrity during DNA Replication. Molecular cell 116 30217558
2019 A consensus set of genetic vulnerabilities to ATR inhibition. Open biology 88 31506018
2018 Polε Instability Drives Replication Stress, Abnormal Development, and Tumorigenesis. Molecular cell 69 29754823
2004 The histone-fold protein complex CHRAC-15/17 enhances nucleosome sliding and assembly mediated by ACF. Molecular cell 63 14759371
2007 Protein binding to lanthanide(III) complexes can reduce the water exchange rate at the lanthanide. Inorganic chemistry 41 17425306
2023 Asymmetric distribution of parental H3K9me3 in S phase silences L1 elements. Nature 37 37938774
2020 CRISPR-based gene knockout screens reveal deubiquitinases involved in HIV-1 latency in two Jurkat cell models. Scientific reports 35 32210344
2018 Total Synthesis, Biological Evaluation, and Target Identification of Rare Abies Sesquiterpenoids. Journal of the American Chemical Society 33 30461272
2020 CRISPR/CAS9-based DNA damage response screens reveal gene-drug interactions. DNA repair 32 31991288
2023 Symmetric inheritance of parental histones contributes to safeguarding the fate of mouse embryonic stem cells during differentiation. Nature genetics 27 37666989
2021 ASF1B Promotes Oncogenesis in Lung Adenocarcinoma and Other Cancer Types. Frontiers in oncology 27 34568067
2018 Iron deficiency accelerates intervertebral disc degeneration through affecting the stability of DNA polymerase epsilon complex. American journal of translational research 22 30662597
2022 Stable inheritance of H3.3-containing nucleosomes during mitotic cell divisions. Nature communications 20 35523900
2018 Orthoxenografts of Testicular Germ Cell Tumors Demonstrate Genomic Changes Associated with Cisplatin Resistance and Identify PDMP as a Resensitizing Agent. Clinical cancer research : an official journal of the American Association for Cancer Research 18 29618620
2000 Cloning and characterization of the histone-fold proteins YBL1 and YCL1. Nucleic acids research 16 11000277
2020 Lymphocyte-Specific Function of the DNA Polymerase Epsilon Subunit Pole3 Revealed by Neomorphic Alleles. Cell reports 15 32553171
2022 MMS22L-TONSL functions in sister chromatid cohesion in a pathway parallel to DSCC1-RFC. Life science alliance 14 36622344
2021 Dpb4 promotes resection of DNA double-strand breaks and checkpoint activation by acting in two different protein complexes. Nature communications 14 34362907
2006 The Pole3 bidirectional unit is regulated by MYC and E2Fs. Gene 11 16403426
2024 Loss of POLE3-POLE4 unleashes replicative gap accumulation upon treatment with PARP inhibitors. Cell reports 10 38753485
2023 Requirement of WDR70 for POLE3-mediated DNA double-strand breaks repair. Science advances 10 37682991
2024 The loss of DNA polymerase epsilon accessory subunits POLE3-POLE4 leads to BRCA1-independent PARP inhibitor sensitivity. Nucleic acids research 7 38828775
2023 POLE3 is a repressor of unintegrated HIV-1 DNA required for efficient virus integration and escape from innate immune sensing. Science advances 7 37922361
2021 Nanoparticle-Encapsulated Camptothecin: Epigenetic Modulation in DNA Repair Mechanisms in Colon Cancer Cells. Molecules (Basel, Switzerland) 5 34500845
2025 'Where is my gap': mechanisms underpinning PARP inhibitor sensitivity in cancer. Biochemical Society transactions 4 39927794
2021 Camptothecin Encapsulated in β-Cyclodextrin-EDTA-Fe3O4 Nanoparticles Induce Metabolic Reprogramming Repair in HT29 Cancer Cells through Epigenetic Modulation: A Bioinformatics Approach. Nanomaterials (Basel, Switzerland) 4 34947512
2025 Proximal proteomics analysis reveals DNA polymerase δ subunit 3 is a new MCM2 binding partner and promotes parental histones inheritance in mammalian cells. Cell death and differentiation 3 41310184
2024 Utilizing an integrated bioinformatics and machine learning approach to uncover biomarkers linking ulcerative colitis to purine metabolism-related genes. Heliyon 2 39524758
2025 Utilizing integrated bioinformatics and machine learning approaches to elucidate biomarkers linking sepsis to purine metabolism-associated genes. Scientific reports 1 39747316
2023 Ln(III) Complexes Embedded in Biocompatible PLGA Nanoparticles as Potential Vis-to-NIR Optical Probes. Molecules (Basel, Switzerland) 1 36903496
2026 USP15 Promotes Pancreatic Cancer Progression and Cisplatin Resistance By Activating DNA Damage Repair. Molecular carcinogenesis 0 41950365
2025 Unveiling Replication Timing-Dependent Mutational Biases: Mechanistic Insights from Gene Knockouts and Genotoxins Exposures. International journal of molecular sciences 0 40806440
2025 Programmable synthesis of alkaloidal frameworks integrating Michael acceptor generates covalent probes for targeting POLE3 in HBV replication. RSC chemical biology 0 41164343
2025 The genetic and biochemical basis of human leading strand synthesis. Nature communications 0 41339636

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