Affinage

POLQ

DNA polymerase theta · UniProt O75417

Length
2590 aa
Mass
289.6 kDa
Annotated
2026-06-10
50 papers in source corpus 20 papers cited in narrative 21 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

POLQ (DNA polymerase theta) is the central effector of theta-mediated/alternative end joining (TMEJ/alt-EJ), a Ku-independent double-strand break (DSB) repair pathway that joins ends through short microhomologies (PMID:25275444). It is a large multidomain enzyme combining an N-terminal single-stranded-DNA-dependent ATPase/helicase domain with a C-terminal family A DNA polymerase domain, and purified full-length protein displays both polymerase activity on primed and nicked templates and ssDNA-dependent ATPase activity (PMID:14576298). The polymerase domain is intrinsically lesion-tolerant: three unique sequence insertions absent from other A-family polymerases (insertions 2 and 3 being essential) enable synthesis on undamaged DNA and bypass of abasic sites and thymine glycol (PMID:21050863), and POLQ extends from mismatched primers and from primers opposite a (6-4) photoproduct, acting as an extender polymerase in concert with pol iota (PMID:17920341). In end joining, POLQ uniquely extends DNA from minimally paired 3' overhangs, generating templated insertions at microhomology junctions, and its polymerase activity drives repair of breaks bearing ~6 nt microhomologies in a pathway distinct from RAD52-dependent long-repeat repair (PMID:25275444, PMID:31381562). The two enzymatic domains cooperate beyond DSBs: the helicase activity displaces RPA from post-replicative ssDNA gaps while the polymerase fills them, and microhomology-mediated gap skipping generates characteristic deletion scars in BRCA1/2-deficient or PARP-inhibited cells (PMID:36455556). POLQ also contributes redundantly with POLbeta to base excision repair of oxidative damage (PMID:17018297), suppresses chromosome translocations and interhomolog recombination by promoting end joining in cis (PMID:25275444, PMID:32873648), and is the principal driver of structural variants at common fragile sites under replication stress (PMID:39505880). POLQ loss is synthetically lethal in HR-deficient cancers, where its inhibition activates cGAS-STING signaling and CD8+ T-cell infiltration (PMID:36976649), and POLQ protein abundance and MMEJ activity are tuned by transcript splicing and protein-stability control by factors including DPPA5A and EWSR1 [PMID:37459543, PMID:bio_10.1101_2025.05.06.651696].

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2003 High

    Established the basic enzymatic identity of POLQ, answering whether the predicted dual-domain protein is biochemically active.

    Evidence Baculovirus expression of full-length human POLQ with in vitro polymerase and ATPase assays plus sequence-based domain analysis

    PMID:14576298

    Open questions at the time
    • Did not define a cellular pathway for either activity
    • No functional role for the helicase/ATPase domain established
  2. 2004 High

    Linked POLQ to genome stability in vivo and to DSB repair pathway architecture by showing genetic interaction with ATM.

    Evidence Mouse chaos1 missense allele characterized by BAC and allelic complementation; Polq/Atm double-mutant phenotyping and micronucleus assays

    PMID:15542845

    Open questions at the time
    • Molecular mechanism of chromosome instability not defined
    • Did not identify the repair pathway POLQ acts in
  3. 2006 High

    Defined a base excision repair role for POLQ redundant with POLbeta, answering which damage types depend on POLQ.

    Evidence DT40 single and double knockouts, in vitro BER assays on extracts, and live-cell imaging of POLQ recruitment to laser damage

    PMID:17018297

    Open questions at the time
    • Precise BER step performed by POLQ not resolved
    • Relationship between BER role and DSB role unclear
  4. 2007 High

    Showed POLQ functions as a lesion-tolerant extender polymerase, explaining how it copes with mismatched and damaged termini.

    Evidence In vitro primer extension on mismatch, CPD and (6-4) photoproduct templates and two-polymerase reconstitution with pol iota

    PMID:17920341

    Open questions at the time
    • In vivo relevance of (6-4) bypass not established
    • Partner insertases in cells not identified
  5. 2010 High

    Identified the structural basis of POLQ's lesion bypass by mapping three unique insertion elements required for activity.

    Evidence Systematic deletion mutagenesis of pol-domain insertions with in vitro TLS assays on abasic and thymine glycol templates

    PMID:21050863

    Open questions at the time
    • No crystal structure of the active insertions
    • Contribution of insertions to end joining not tested here
  6. 2011 Medium

    Separated functions of POLQ's polymerase and non-polymerase domains, showing the helicase-like region has independent activity in DSB-agent tolerance.

    Evidence POLQ-null versus pol-domain-deleted CH12F3 B cells with clonogenic survival across multiple damaging agents and CSR assays

    PMID:21883722

    Open questions at the time
    • Biochemical function of the non-polymerase domain in survival undefined
    • Single cell-line system
  7. 2014 High

    Defined POLQ as the effector of Ku-independent alt-EJ that uses minimally paired primers and suppresses translocations, establishing the core TMEJ mechanism.

    Evidence Polq-null murine cells, long-3'-overhang end-joining substrates, CSR and Ku70-independent assays, purified-protein biochemistry, and translocation PCR

    PMID:25275444

    Open questions at the time
    • End resection factors feeding POLQ not defined
    • Ligase used to seal POLQ-extended ends not identified here
  8. 2016 Medium

    Showed alt-EJ via POLQ is the dominant DSB repair route in early vertebrate development, establishing physiological importance.

    Evidence Zebrafish polq mutants with CRISPR/Cas9- and irradiation-induced DSBs, survival and mutation-spectrum analysis

    PMID:27149851

    Open questions at the time
    • Developmental-stage specificity of dependence not mechanistically explained
    • Single model organism
  9. 2017 Medium

    Demonstrated POLQ mediates homology-independent foreign-DNA integration as the sole route when NHEJ is absent.

    Evidence POLQ/LIG4 double-knockout human cells with random integration and gene targeting frequency assays

    PMID:28695890

    Open questions at the time
    • Mechanism of capturing exogenous DNA ends not detailed
    • Single lab
  10. 2019 Medium

    Connected POLQ to replication-associated breaks and distinguished its microhomology preference from RAD52's, refining pathway boundaries.

    Evidence POLQ-deficient and RAD52-knockout human cells with defined-microhomology DSB substrates, fork-restart assays, and survival with TOP/ATR inhibitors

    PMID:30655289 PMID:31381562

    Open questions at the time
    • How POLQ is recruited specifically to collapsed forks unclear
    • Determinants of microhomology length selection not molecularly defined
  11. 2020 Medium

    Showed POLQ enforces cis end-joining to suppress interhomolog recombination and copy-neutral LOH, explaining its anti-recombinogenic role.

    Evidence POLQ depletion with CRISPR-Cas9 DSBs on both homologs and quantitative IHR/cnLOH assays in human cells

    PMID:32873648

    Open questions at the time
    • Mechanism restricting break mobility not defined
    • Depletion rather than clean genetic null
  12. 2022 High

    Defined a post-replicative ssDNA gap-sealing function in BRCA-deficient cells, reconstituting cooperation between the helicase (RPA displacement) and polymerase (gap fill-in) activities.

    Evidence POLQ-deficient cells with BRCA1/2 loss or PARP inhibition, gap-accumulation assays, biochemical reconstitution of both domain activities, and genomic-scar analysis

    PMID:36455556

    Open questions at the time
    • Trigger directing POLQ to gaps versus DSBs unclear
    • MMGS choice between fill-in and skipping not regulated mechanistically
  13. 2023 Medium

    Showed POLQ inhibition in HR-deficient tumors is synthetically lethal and engages cGAS-STING-driven anti-tumor immunity, providing therapeutic mechanism.

    Evidence POLQ knockdown in HR-deficient PDAC models, synthetic-lethality and micronuclei assays, cGAS-STING readouts, and in vivo CD8+ T-cell quantification

    PMID:36976649

    Open questions at the time
    • Source of immunogenic cytosolic DNA not fully traced to POLQ activity
    • Single tumor type
  14. 2023 Medium

    Revealed transcript-level control of POLQ via DPPA5A-driven cryptic exon inclusion that suppresses POLθ expression and MMEJ.

    Evidence DPPA5A depletion and overexpression in mouse ESCs and NIH3T3 with RT-PCR, Western blot, and MMEJ assays

    PMID:37459543

    Open questions at the time
    • Direct binding of DPPA5A to Polq pre-mRNA not shown here
    • Human relevance untested
  15. 2024 Medium

    Established POLQ as the principal driver of nonrecurrent structural variants at common fragile sites under replication stress.

    Evidence Error-minimized capture sequencing of CFS DNA after aphidicolin, pathway inhibition, and cell-cycle fractionation in human cells

    PMID:39505880

    Open questions at the time
    • Why SV formation peaks after G2-to-M not mechanistically explained
    • Pharmacological rather than genetic POLQ loss
  16. 2025 Medium

    Identified multiple convergent mechanisms controlling POLQ protein stability and splicing accuracy in cancer contexts (HPV16 E6/UBE3A/RAD23A, EWSR1/EWS-FLI1, SMARCB1).

    Evidence HPV16 E6 and UBE3A/RAD23A perturbations, EWSR1/EWS-FLI1 splicing assays, and SMARCB1-deficient cell analyses with MMEJ readouts (preprints)

    PMID:41357977 PMID:bio_10.1101_2025.05.06.651696 PMID:bio_10.1101_2025.11.20.689563

    Open questions at the time
    • Mechanisms are preprint-stage and single-lab
    • Nuclear-export mechanism for POLQ mRNA inferred without reconstitution
    • Generality across tumor types untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How POLQ is recruited to and selects among its substrates (DSB ends, post-replicative gaps, fragile sites) and which factors hand off ends to and seal POLQ-extended products remain unresolved.
  • No structural model of full-length POLQ engaging a substrate
  • Recruitment and substrate-choice determinants undefined
  • Ligation partner sealing POLQ-extended junctions not identified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 4 GO:0003677 DNA binding 2 GO:0016787 hydrolase activity 2 GO:0140657 ATP-dependent activity 2
Localization
GO:0005634 nucleus 2
Pathway
R-HSA-73894 DNA Repair 3 R-HSA-1643685 Disease 2
Partners
DPPA5AEWSR1POLBRAD23ARAD52SMARCB1UBE3A

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 POLQ encodes a 2592-amino acid protein with an N-terminal ATPase-helicase domain, a central spacer domain, and a C-terminal family A DNA polymerase domain. Purified full-length human POLQ displays DNA polymerase activity on nicked double-stranded DNA and singly primed templates (resistant to aphidicolin, inhibited by dideoxynucleotides) and a single-stranded DNA-dependent ATPase activity. Baculovirus expression and purification of full-length human POLQ; in vitro polymerase and ATPase assays; domain analysis by sequence Nucleic acids research High 14576298
2010 The DNA polymerase (pol) domain of POLQ is sufficient for highly efficient bypass of abasic sites, independent of the helicase-like or central domains. Three unique sequence insertions (not found in other A-family polymerases) are required for lesion bypass: insertion 1 increases processivity but does not affect TLS; insertions 2 and 3 are essential for activity on undamaged DNA and completely required for bypass of abasic sites and thymine glycol lesions. In vitro polymerase assay with purified recombinant POLQ pol domain deletion constructs lacking each insertion element individually; translesion synthesis assays on abasic site and thymine glycol templates Journal of molecular biology High 21050863
2007 POLQ (pol theta) can extend DNA from mismatched termini (A:G, A:T, A:C mismatches) with less discrimination than E. coli pol I, and can extend from primers placed opposite a (6-4) photoproduct. When combined with DNA polymerase iota (which inserts opposite the lesion), POLQ enables complete bypass of a (6-4) photoproduct, acting as an extender polymerase. In vitro primer extension assays with purified POLQ on templates containing mismatches, cyclobutane pyrimidine dimers, and (6-4) photoproducts; two-polymerase reconstitution with pol iota + POLQ DNA repair High 17920341
2006 POLQ participates in base excision repair (BER) of oxidative DNA damage and has an overlapping function with POLbeta. POLQ-deficient DT40 cells are hypersensitive to H2O2-induced oxidative base damage; this is synergistically enhanced by concurrent POLbeta deletion. Cell extracts from POLQ-null cells show reduced BER activity. POLQ accumulates rapidly at sites of base damage, similar to POLbeta. Gene disruption in chicken DT40 cells (POLQ, POLbeta, polq/polb double mutants); cell survival assays; in vitro BER activity assays on cell extracts; live-cell imaging of POLQ accumulation at laser-induced damage sites Molecular cell High 17018297
2014 POLQ mediates an alternative end-joining (alt-EJ) pathway for DNA double-strand break repair that is Ku70-independent and requires POLQ's DNA polymerase activity. POLQ promotes end joining of DNA ends with long 3' single-stranded overhangs by its unique ability to extend DNA from minimally paired primers, generating insertions of base pairs at joins with microhomology to switch-region sequences. Loss of POLQ leads to increased Myc/IgH chromosome translocations, showing POLQ suppresses genomic instability at DSBs. Polq-null murine cell lines; cell-based DNA break end-joining assay with long 3' ssDNA overhang substrates; immunoglobulin class switch recombination assays; Ku70-independent assay; biochemical assays with purified human POLQ; chromosomal translocation analysis by PCR PLoS genetics High 25275444
2004 The chaos1 missense mutation in mouse Polq causes spontaneous and induced chromosome instability (increased micronucleated erythrocytes). Chaos1 is confirmed as a Polq allele by BAC complementation and failed complementation with a Polq-null allele. Double homozygosity with Atm deficiency is synthetically lethal (90% neonatal death), with survivors showing synergistic growth retardation and chromosome instability, indicating that POLQ and ATM operate in distinct but partially compensatory DSB repair pathways. Mouse genetics: BAC complementation, allelic complementation test with gene-targeted Polq null; double-mutant (Polq/Atm) phenotypic analysis; micronucleus assay Molecular and cellular biology High 15542845
2011 POLQ's non-polymerase domains retain significant function in tolerance to DSB-inducing agents (etoposide, gamma-irradiation): POLQ-null B cells are more sensitive than POLQ-polymerase-inactive (pol domain deleted) cells to these agents, while both are equally sensitive to agents repaired by the polymerase domain (MMC, cisplatin, UV). Class switch recombination is unaffected by loss of either form of POLQ. Gene targeting in CH12F3 B cells to generate POLQ-null and POLQ-polymerase-inactive lines; clonogenic survival assays with multiple DNA-damaging agents; class switch recombination assay Genes to cells Medium 21883722
2016 In zebrafish embryos, POLQ-mediated alternative end joining (alt-EJ) is the essential and dominant pathway for repair of DSBs during early vertebrate development. Polq-mutant embryos cannot repair CRISPR/Cas9- or ionizing radiation-induced DSBs, fail to survive mutagenesis, and show dramatic differences in mutation profiles compared to wild-type. Zebrafish polq genetic mutants; CRISPR/Cas9-induced DSBs; ionizing radiation; survival assays; mutation spectrum analysis Cell reports Medium 27149851
2017 POLQ substantially contributes to random integration of foreign DNA in human cells via a mechanism independent of NHEJ. Dual loss of POLQ and LIG4 (essential for NHEJ) abolishes random integration entirely, revealing that POLQ-mediated end joining is the sole homology-independent repair route for foreign DNA integration when NHEJ is absent. POLQ and LIG4 double-knockout human cells; gene targeting frequency assays; random integration frequency measurement Nature communications Medium 28695890
2019 POLQ is required for MMEJ repair of DSBs generated by both endonucleases (I-SceI, Cas9) and Cas9 nickase-derived single-strand breaks that collapse at replication forks. POLQ deficiency causes sensitivity to topoisomerase inhibitors and ATR inhibitors that induce replication stress and fork collapse, placing POLQ in the response to replication-associated DSBs. POLQ-deficient human cancer cell lines; I-SceI and Cas9/Cas9-nickase DSB repair assays; clonogenic survival with topoisomerase inhibitors and ATR inhibitors The Journal of biological chemistry Medium 30655289
2019 POLQ and RAD52 operate in distinct backup DSB repair pathways with different microhomology requirements: POLQ is important for repair events using 6 nt (but not ≥18 nt) flanking microhomologies and for oligonucleotide microhomology-templated (12–20 nt) repair events requiring nascent DNA synthesis, whereas RAD52 is important for longer (≥50 nt) repeat-mediated repair. Combined disruption of both causes additive hypersensitivity to cisplatin and synthetic reduction in replication fork restart velocity. Human U2OS cells with POLQ mutations (upstream of pol domain), RAD52 knockout, and combined disruption; defined DSB repair substrate assays; fork restart assay; clonogenic survival PLoS genetics Medium 31381562
2022 POLQ seals post-replicative ssDNA gaps in BRCA1/2-deficient cells or upon PARP inhibitor treatment. Biochemically, the POLQ helicase activity promotes RPA displacement from ssDNA gaps while the polymerase activity fills in the gaps. POLQ also performs microhomology-mediated gap skipping (MMGS), generating deletions during gap repair that resemble genomic scars in POLQ-overexpressing cancers. POLQ-deficient cell lines with BRCA1/2 loss or PARP inhibitor treatment; ssDNA gap accumulation assay; biochemical reconstitution of RPA displacement and gap fill-in with POLQ helicase and polymerase domain activities; genomic scar analysis Molecular cell High 36455556
2020 POLQ promotes end joining in cis at DSBs, limiting breaks available for interhomolog recombination (IHR) in trans. Depletion of POLQ causes a dramatic increase in IHR and in copy-neutral loss of heterozygosity (cnLOH) at CRISPR-Cas9-targeted DSBs in human cells. POLQ depletion in human cells; CRISPR-Cas9 targeted DSBs at both homologs; quantitative IHR and cnLOH frequency assays Proceedings of the National Academy of Sciences of the United States of America Medium 32873648
2008 In C. elegans, polq-1 functions in a distinct ICL repair pathway that is dependent on brc-1 (CeBRCA1), separate from the Fanconi anemia-dependent pathway used by hel-308. Epistasis analysis places polq-1 and hel-308 in different DNA repair pathways. C. elegans polq-1 and hel-308 mutants; survival assays after ICL agent treatment; genetic epistasis analysis with Fanconi anemia pathway mutants and brc-1 DNA repair Medium 18472307
2024 POLQ-mediated end-joining (TMEJ) is the primary mechanism generating structural variants (SVs) at common fragile sites (CFSs) in human cells under replication stress. SV junction formation increases 5-fold after G2-to-M-phase transition; neither SV formation nor CFS expression depend on mitotic DNA synthesis (MiDAS). POLQ inhibition reduces SV formation, placing POLQ as the principal driver of nonrecurrent SV formation at CFSs. Error-minimized capture sequencing of CFS DNA from human cell lines after aphidicolin treatment; DNA repair pathway inhibition (POLQ and others); cell cycle fractionation; analysis of tens of thousands of de novo SV junctions Nature communications Medium 39505880
2023 POLQ inhibition in HR-deficient BRCA2-deficient pancreatic cancer cells is synthetically lethal and activates cGAS-STING signaling by enhancing cytosolic micronuclei formation, leading to increased CD8+ T cell infiltration in vivo. POLQ knockdown in human and murine HR-deficient PDAC models; synthetic lethality assay with BRCA1/2 and ATM mutations; micronuclei quantification; cGAS-STING signaling assay; in vivo syngeneic tumor model with CD8+ T cell quantification The Journal of clinical investigation Medium 36976649
2023 In mouse embryonic stem cells, the RNA-binding protein DPPA5A promotes cryptic exon (CE) inclusion in Polq pre-mRNA, disrupting normal POLθ protein expression and suppressing MMEJ activity. Depletion of DPPA5A decreases CE inclusion in Polq, restores POLθ expression, and stimulates MMEJ activity. DPPA5A depletion in mouse ESCs; RT-PCR for CE inclusion in Polq; Western blot for POLθ protein; MMEJ activity assays; enforced DPPA5A expression in NIH3T3 cells Proceedings of the National Academy of Sciences of the United States of America Medium 37459543
2025 HPV16 E6 oncoprotein stabilizes POLQ protein by activating the E3 ubiquitin ligase UBE3A/E6AP, which ubiquitinates and degrades RAD23A — a shuttle protein required for delivering polyubiquitinated POLQ to the proteasome. Loss of RAD23A phenocopies HPV16 E6 expression, leading to POLQ stabilization and increased MMEJ activity. This E6-UBE3A-RAD23A-POLQ axis promotes viral genome integration. Co-expression of HPV16 E6 in cells; Western blot for POLQ and RAD23A protein levels; UBE3A knockdown/knockout; RAD23A knockdown; MMEJ activity assays; viral integration assays; ubiquitination assays bioRxivpreprint Medium 41357977
2025 SMARCB1 (a core BAF/SWI-SNF subunit) is required for maintaining POLQ protein levels by facilitating nuclear export of POLQ mRNA through interaction with the nuclear pore complex. Loss of SMARCB1 reduces POLQ protein, impairs MMEJ, and forces a compensatory hyper-dependence on the FA/BRCA pathway. SMARCB1-deficient rhabdoid tumor cell lines; Western blot for POLQ protein; POLQ mRNA nuclear export assay; nuclear pore complex interaction; MMEJ activity assay; synthetic lethality with FA/BRCA pathway inhibition bioRxivpreprint Low bio_10.1101_2025.11.20.689563
2025 EWSR1 is a splicing factor that promotes accurate splicing of POLQ pre-mRNA. The EWS-FLI1 fusion oncoprotein, or loss of EWSR1, causes exon 25 skipping of the POLQ transcript, decreased POLθ protein expression, and impaired MMEJ activity in Ewing sarcoma cells. Knockdown of EWS-FLI1 restores POLθ expression and increases MMEJ activity. Ewing sarcoma cell lines with EWS-FLI1 expression or EWSR1 loss; RT-PCR for POLQ exon 25 skipping; Western blot for POLθ; MMEJ activity assay; EWS-FLI1 knockdown rescue experiments; POLQ mitotic foci quantification bioRxivpreprint Medium bio_10.1101_2025.05.06.651696
2025 POLQ variant forms (patient-derived melanoma variants) show decreased efficiency during bypass and extension of cyclobutane pyrimidine dimers (CPDs) compared to wild-type, but two of three tested variants nonetheless protect against UV-induced cell death, dissociating lesion bypass efficiency from cell survival. In vitro primer extension assays with purified recombinant POLQ variants on CPD-containing templates; cell survival assays after UV irradiation with POLQ variant expression bioRxivpreprint Low 41357977

Source papers

Stage 0 corpus · 50 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Mechanism of suppression of chromosomal instability by DNA polymerase POLQ. PLoS genetics 245 25275444
2003 POLQ (Pol theta), a DNA polymerase and DNA-dependent ATPase in human cells. Nucleic acids research 182 14576298
2016 DNA polymerase θ (POLQ), double-strand break repair, and cancer. DNA repair 178 27264557
2004 The mouse genomic instability mutation chaos1 is an allele of Polq that exhibits genetic interaction with Atm. Molecular and cellular biology 127 15542845
2010 A small interfering RNA screen of genes involved in DNA repair identifies tumor-specific radiosensitization by POLQ knockdown. Cancer research 114 20233878
2006 Vertebrate POLQ and POLbeta cooperate in base excision repair of oxidative DNA damage. Molecular cell 114 17018297
2022 POLQ seals post-replicative ssDNA gaps to maintain genome stability in BRCA-deficient cancer cells. Molecular cell 105 36455556
1999 Cloning and chromosomal mapping of the human DNA polymerase theta (POLQ), the eighth human DNA polymerase. Genomics 99 10395804
2012 DNA replication stress response involving PLK1, CDC6, POLQ, RAD51 and CLASPIN upregulation prognoses the outcome of early/mid-stage non-small cell lung cancer patients. Oncogenesis 98 23552402
2010 Lesion bypass activity of DNA polymerase θ (POLQ) is an intrinsic property of the pol domain and depends on unique sequence inserts. Journal of molecular biology 93 21050863
2019 DNA polymerase θ (POLQ) is important for repair of DNA double-strand breaks caused by fork collapse. The Journal of biological chemistry 92 30655289
2008 Caenorhabditis elegans POLQ-1 and HEL-308 function in two distinct DNA interstrand cross-link repair pathways. DNA repair 86 18472307
2012 DNA polymerase POLQ and cellular defense against DNA damage. DNA repair 85 23219161
2017 Dual loss of human POLQ and LIG4 abolishes random integration. Nature communications 78 28695890
2007 DNA polymerase theta (POLQ) can extend from mismatches and from bases opposite a (6-4) photoproduct. DNA repair 77 17920341
2009 Lack of DNA polymerase theta (POLQ) radiosensitizes bone marrow stromal cells in vitro and increases reticulocyte micronuclei after total-body irradiation. Radiation research 67 19630521
2019 Distinct roles of RAD52 and POLQ in chromosomal break repair and replication stress response. PLoS genetics 65 31381562
2023 POLQ inhibition elicits an immune response in homologous recombination-deficient pancreatic adenocarcinoma via cGAS/STING signaling. The Journal of clinical investigation 54 36976649
2016 Polq-Mediated End Joining Is Essential for Surviving DNA Double-Strand Breaks during Early Zebrafish Development. Cell reports 51 27149851
2019 POLQ plays a key role in the repair of CRISPR/Cas9-induced double-stranded breaks in the moss Physcomitrella patens. The New phytologist 37 30636294
2019 POLQ Overexpression Is Associated with an Increased Somatic Mutation Load and PLK4 Overexpression in Lung Adenocarcinoma. Cancers 32 31137743
2024 Iron promotes ovarian cancer malignancy and advances platinum resistance by enhancing DNA repair via FTH1/FTL/POLQ/RAD51 axis. Cell death & disease 30 38740757
2021 Knockdown of POLQ interferes the development and progression of hepatocellular carcinoma through regulating cell proliferation, apoptosis and migration. Cancer cell international 22 34517891
2020 POLQ suppresses interhomolog recombination and loss of heterozygosity at targeted DNA breaks. Proceedings of the National Academy of Sciences of the United States of America 21 32873648
2017 Expression and Structural Analyses of Human DNA Polymerase θ (POLQ). Methods in enzymology 19 28668117
2021 Chlamydomonas POLQ is necessary for CRISPR/Cas9-mediated gene targeting. G3 (Bethesda, Md.) 18 33836052
2024 POLQ inhibition attenuates the stemness and ferroptosis resistance in gastric cancer cells via downregulation of dihydroorotate dehydrogenase. Cell death & disease 17 38575587
2018 Helicase POLQ-like (HELQ) as a novel indicator of platinum-based chemoresistance for epithelial ovarian cancer. Gynecologic oncology 16 29572031
2014 A DNA repair variant in POLQ (c.-1060A > G) is associated to hereditary breast cancer patients: a case-control study. BMC cancer 13 25409685
2011 Comparison of two POLQ mutants reveals that a polymerase-inactive POLQ retains significant function in tolerance to etoposide and γ-irradiation in mouse B cells. Genes to cells : devoted to molecular & cellular mechanisms 12 21883722
2024 Replication stress induces POLQ-mediated structural variant formation throughout common fragile sites after entry into mitosis. Nature communications 11 39505880
2022 Whole-exome sequencing of Indian prostate cancer reveals a novel therapeutic target: POLQ. Journal of cancer research and clinical oncology 11 35737091
2019 Hypersensitivity to DNA double-strand breaks associated with PARG deficiency is suppressed by exo-1 and polq-1 mutations in Caenorhabditis elegans. The FEBS journal 10 31593615
2023 DPPA5A suppresses the mutagenic TLS and MMEJ pathways by modulating the cryptic splicing of Rev1 and Polq in mouse embryonic stem cells. Proceedings of the National Academy of Sciences of the United States of America 8 37459543
2022 POLQ suppresses genome instability and alterations in DNA repeat tract lengths. NAR cancer 8 35774233
2024 POLQ identifies a better response subset to immunotherapy in muscle-invasive bladder cancer with high PD-L1. Cancer medicine 7 38457207
2024 The m6A demethylase FTO targets POLQ to promote ccRCC cell proliferation and genome stability maintenance. Journal of cancer research and clinical oncology 5 38270643
2024 Induction of the DNA-Repair Gene POLQ only in BRCA1-mutant Breast-Cancer Cells by Methionine Restriction. Cancer genomics & proteomics 4 38944428
2020 Mutant POLQ and POLZ/REV3L DNA polymerases may contribute to the favorable survival of patients with tumors with POLE mutations outside the exonuclease domain. BMC medical genetics 4 32838755
2025 FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations. Nature communications 3 40082407
2024 POLQ knockdown inhibits proliferation, migration, and invasion by inducing cell cycle arrest in colorectal cancer. Discover oncology 2 39520627
2025 Preparation of Substituted Heterocycles and Their Use as DNA Polymerase Theta (POLQ) Inhibitors. ACS medicinal chemistry letters 1 40236543
2025 Identification and Targeting of POLQ-Associated Hereditary Colorectal Cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 1 40423529
2025 POLQ mediated end-joining promotes DNA damage tolerance in neuroblastoma. Translational oncology 1 40482467
2026 POLQ promotes tumor progression and immunosuppression via ATM‑P53 signaling in endometrial cancer. Oncology reports 0 41823540
2026 POLQ-driven repair scars shape the immunogenic landscape of homologous recombination-deficient pancreatic cancer. bioRxiv : the preprint server for biology 0 41889863
2026 The Potential of DNA Polymerase Theta (POLQ) Inhibitors as Cancer Therapy for Homologous Recombination (HR)-Deficient Tumors. ACS medicinal chemistry letters 0 41982723
2025 POLQ and DNA-PK inhibition in muscle-invasive bladder cancer : Enhancing radiosensitivity with novel DNA damage response inhibitors to improve radiotherapy outcomes. Pathologie (Heidelberg, Germany) 0 41295990
2025 POLQ variants with aberrant DNA polymerase activity protect against UV-induced cell death. bioRxiv : the preprint server for biology 0 41357977
2023 [Study on enhanced sensitivity to DNA damage in POLQ knocking-down salivary of adenoid cystic carcinoma-83 cells]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 37153990

Missed literature

Know a paper Affinage missed for POLQ? Flag it for the maintainers and the community.

No submissions yet.