Affinage

POLB

DNA polymerase beta · UniProt P06746

Round 2 corrected
Length
335 aa
Mass
38.2 kDa
Annotated
2026-04-28
69 papers in source corpus 16 papers cited in narrative 16 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DNA polymerase beta (POLB) is the principal gap-filling polymerase in the base excision repair (BER) pathway, possessing a bifunctional architecture: an N-terminal 8-kDa domain that catalyzes 5′-deoxyribose phosphate (dRP) excision via a Lys72-dependent Schiff base lyase mechanism, and a C-terminal 31-kDa polymerase domain that employs an induced-fit mechanism—thumb subdomain closure upon correct nucleotide binding coupled to transient formation of a third active-site metal—to fill single-nucleotide gaps with high fidelity (PMID:9614142, PMID:9287163, PMID:23827680). POLB operates within a BER scaffold coordinated by XRCC1, which suppresses strand displacement and links pol β to DNA ligase III and PNK, and receives substrate via sequential handoff from APE1 or, in an APE1-independent sub-pathway, from NEIL1/PNK for oxidized-base lesions (PMID:8978692, PMID:9207062, PMID:15260972). POLB also localizes to mitochondria where it contributes to mitochondrial DNA integrity (PMID:29129598). A hypomorphic Y265C allele in mice causes accumulation of BER intermediates and a lupus-like autoimmune disease driven by aberrant immunoglobulin diversification in hematopoietic cells, and simultaneous loss of both POLB catalytic activities is synthetically lethal with PARP inhibition in BRCA1/2-deficient cancers (PMID:24388753, PMID:34186496, PMID:40326293).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1986 Medium

    Chromosomal localization of the human POLB gene to chromosome 8 established the genomic foundation for subsequent molecular studies.

    Evidence Southern blot hybridization of human-mouse somatic cell hybrids using a rat pol β cDNA probe

    PMID:3009375

    Open questions at the time
    • No functional characterization at this stage
    • Cross-species probe may miss structural nuances of the human locus
  2. 1996 High

    Structural and biochemical studies revealed the dual-domain architecture of pol β—an 8-kDa HhH DNA-binding lyase domain and a 31-kDa polymerase domain—and its direct interaction with XRCC1, which suppresses strand displacement to ensure single-nucleotide patch BER and coordinates pol β with DNA ligase III.

    Evidence X-ray crystallography of pol β–DNA binary complexes; far Western, affinity precipitation, yeast two-hybrid, and reconstituted BER assays

    PMID:8841118 PMID:8978692

    Open questions at the time
    • Ternary complex with dNTP not yet captured
    • Structural basis of XRCC1-mediated strand-displacement suppression unresolved
  3. 1997 High

    Crystal structures of pol β at multiple catalytic stages demonstrated an induced-fit mechanism—thumb closure upon correct dNTP binding triggering catalytic alignment—and showed that APE1 physically hands off incised AP-DNA to pol β, kinetically accelerating dRP excision in a coordinated BER handoff.

    Evidence X-ray crystallography of binary, ternary (ddCTP), and product complexes at 2.2–2.6 Å; yeast two-hybrid and steady-state kinetics with APE1

    PMID:9207062 PMID:9287163

    Open questions at the time
    • Natural substrates not yet used in crystallographic studies
    • Third metal site not identified at this resolution
  4. 1998 High

    Kinetic dissection established that the isolated 8-kDa domain is sufficient for both dRP lyase and AP lyase activities, with Lys72 acting as a Schiff base nucleophile, and that the dRP lyase rate on pre-incised substrates vastly exceeds AP lyase activity on intact sites.

    Evidence Steady-state kinetics with full-length and 8-kDa domain; pyridoxal 5′-phosphate inhibition and Mg²⁺ omission experiments

    PMID:9614142

    Open questions at the time
    • Crystal structure of Schiff base intermediate not captured
    • Contribution of lyase vs. polymerase activity to overall BER flux in cells not quantified
  5. 2001 High

    Identification of PNK as a fourth component of the XRCC1 scaffold complex expanded the BER model to include processing of damaged DNA termini, with XRCC1 stimulating PNK's kinase and phosphatase activities.

    Evidence Co-immunoprecipitation from human cell extracts; reconstituted kinase/phosphatase and repair assays

    PMID:11163244

    Open questions at the time
    • Structural basis of XRCC1–PNK–pol β ternary complex unknown
    • Relative contribution of PNK-dependent sub-pathway in vivo not measured
  6. 2004 High

    Discovery that NEIL1 DNA glycosylase stably associates with pol β and DNA ligase IIIα defined an APE1-independent BER sub-pathway for oxidized bases generating 3′-phosphate termini, where PNK replaces APE1 for end processing.

    Evidence Co-immunoprecipitation and reconstituted repair assays with purified NEIL1, pol β, PNK, and ligase IIIα

    PMID:15260972

    Open questions at the time
    • Relative physiological flux through APE1-dependent vs. NEIL1/PNK-dependent BER unknown
    • Structural model of the NEIL1–pol β complex lacking
  7. 2012 Medium

    Sequencing of colorectal tumors revealed POLB coding mutations in ~40% of samples, with a subset showing reduced polymerase activity and failure to rescue BER-deficient cells, implicating somatic pol β dysfunction in tumorigenesis.

    Evidence POLB sequencing of 134 tumors; in vitro enzyme assays and MMS rescue in pol β-null cells

    PMID:22577134

    Open questions at the time
    • Single-lab observation; independent replication in larger cohorts needed
    • Causal role of POLB mutations in tumor initiation vs. progression not distinguished
  8. 2013 High

    Real-time crystallography with natural substrates captured 15 intermediates and identified a transient third metal ion that forms selectively during correct nucleotide insertion, providing a structural basis for polymerase fidelity.

    Evidence Real-time X-ray crystallography with natural dNTP substrates (correct and incorrect)

    PMID:23827680

    Open questions at the time
    • Role of third metal in catalysis vs. fidelity checking not fully separated
    • Whether third metal mechanism is conserved in other X-family polymerases not tested
  9. 2014 High

    A pol β Y265C hypomorphic knockin mouse developed lupus-like autoimmunity with altered immunoglobulin junctions and increased somatic hypermutation, establishing that insufficient pol β catalytic activity during immune diversification drives systemic autoimmune disease.

    Evidence POLB-Y265C knockin mouse; immunological, histopathological, and antibody repertoire analysis

    PMID:24388753

    Open questions at the time
    • Precise stage of B-cell development at which pol β deficiency is pathogenic not defined
    • Whether human POLB variants similarly predispose to SLE not tested
  10. 2017 Medium

    Two independent groups demonstrated that pol β localizes to mitochondria and contributes to mitochondrial BER and mtDNA integrity, overturning the assumption that it is exclusively nuclear.

    Evidence Subcellular fractionation and mitochondrial localization assays with functional mtDNA integrity readouts

    PMID:29129598

    Open questions at the time
    • Mitochondrial import signal or mechanism not identified
    • Relative contribution of pol β vs. pol γ to mtBER not quantified
  11. 2021 High

    Genetic epistasis experiments placing pol β downstream of NEIL1 and OGG1 glycosylases showed that deletion of these glycosylases reduced BER intermediate accumulation and ameliorated lupus-like disease in Y265C mice, confirming that toxic BER intermediates—not loss of repair per se—drive autoimmune pathology.

    Evidence Double-knockout mouse models (PolbY265C × Neil1−/− × Ogg1−/−); antinuclear antibody and renal histopathology

    PMID:34186496

    Open questions at the time
    • Identity of the specific toxic intermediate(s) not characterized
    • Whether additional glycosylases contribute to the pathogenic flux not tested
  12. 2022 Medium

    Bone marrow transplantation proved that the hematopoietic compartment alone is sufficient to transfer lupus-like disease from POLB Y265C mice to wild-type recipients, pinpointing the immune system as the pathogenic cell of origin.

    Evidence Bone marrow transplantation into congenic wild-type mice with ANA and renal pathology readouts

    PMID:35486639

    Open questions at the time
    • Specific hematopoietic lineage responsible (B cells vs. other) not resolved
    • Single-lab study
  13. 2024 Medium

    Development of a duplexed high-throughput assay simultaneously measuring pol β lyase and polymerase activities enabled screening of 200,000 compounds and confirmed that dual inhibition of both activities is required for synthetic lethality with PARPi in BRCA1/2-mutant cells.

    Evidence SAMDI mass spectrometry dual-activity assay; BRCA1/2-mutant cell KO/rescue studies

    PMID:39094983

    Open questions at the time
    • No clinical-grade dual inhibitor yet reported
    • Whether lyase-selective or polymerase-selective inhibitors have therapeutic utility alone not tested
  14. 2025 High

    CRISPR screens and in vivo xenograft validation established POLB as a synthetic lethal partner of PARP inhibitors specifically in BRCA1/2-deficient cancers, with both catalytic activities required for the interaction, opening a therapeutic strategy.

    Evidence CRISPR screens; POLB KO and overexpression of catalytic mutants; murine xenograft models with niraparib

    PMID:40326293

    Open questions at the time
    • Whether synthetic lethality extends to other HR-deficient genotypes beyond BRCA1/2 not tested
    • In vivo toxicity of systemic pol β inhibition not assessed
    • No selective pol β inhibitor has entered clinical development

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the identity and structure of the mitochondrial targeting mechanism for pol β, the precise toxic BER intermediate driving autoimmunity, whether human POLB polymorphisms predispose to lupus, and whether a clinically viable dual-activity pol β inhibitor can be developed for BRCA-deficient cancers.
  • Mitochondrial import mechanism unknown
  • Structure of pathogenic BER intermediate not defined
  • Human genetic association with autoimmunity not established
  • No clinical-grade pol β inhibitor available

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 5 GO:0003677 DNA binding 2 GO:0016829 lyase activity 2
Localization
GO:0005634 nucleus 5 GO:0005739 mitochondrion 1
Pathway
R-HSA-73894 DNA Repair 8 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3
Partners
APEX1LIG3NEIL1OGG1PNKPXRCC1
Complex memberships
NEIL1–pol β–DNA ligase IIIα–PNK complexXRCC1–pol β–DNA ligase III BER complex

Evidence

Reading pass · 16 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 Human DNA polymerase beta (pol β) was shown to directly interact with XRCC1 via the N-terminal region of XRCC1 (residues 84–183), as demonstrated by far Western blotting, affinity precipitation, and yeast two-hybrid analyses. XRCC1 suppresses strand displacement by pol β during BER, allowing efficient ligation after single-nucleotide gap filling, and functions as a scaffold protein coordinating pol β and DNA ligase III in the BER pathway. Far Western blotting, affinity precipitation, yeast two-hybrid, gel retardation assay, reconstituted BER system with purified human proteins The EMBO journal High 8978692
1996 Crystal structures of human pol β complexed with blunt-ended DNA revealed that the 8-kDa domain contains a helix-hairpin-helix (HhH) motif that binds DNA similarly to the HhH motif in the 31-kDa domain, with metal ion facilitation. The 8-kDa domain was shown to harbor a lysine-rich binding pocket for the 5'-phosphate end of gapped DNA. A 90° kink in the DNA at the 5'-phosphodiester of the templating residue was identified as a structural feature enabling pol β to complete gap-filling to a single nucleotide. X-ray crystallography (human pol β–DNA binary complexes) Biochemistry High 8841118
1997 Crystal structures of human pol β in complex with gapped DNA, ternary complex with ddCTP, and nicked product DNA revealed an induced-fit mechanism: upon correct nucleotide binding, the thumb subdomain rotates to the closed conformation, triggering alignment of catalytic residue Asp192, dNTP, and template for nucleotidyl transfer. After synthesis, the thumb returns to open conformation to facilitate product dissociation. A 90° DNA kink at the 5'-phosphodiester of the templating residue was confirmed as essential for thumb–dNTP contact. X-ray crystallography at 2.2–2.6 Å resolution (binary, ternary, and product complexes) Biochemistry High 9287163
1997 Human AP endonuclease (APE/APE1) physically interacts with pol β as shown by yeast two-hybrid analysis. In vitro, APE bound to an uncleaved AP site loads pol β into a ternary APE–pol β–AP-DNA complex; after APE incision, pol β stably binds the DNA. APE kinetically accelerates the excision of the 5'-terminal deoxyribose 5-phosphate (dRP) by pol β, demonstrating coordinated sequential handoff between these two central BER enzymes. Yeast two-hybrid, gel retardation/supershift assays, steady-state kinetics in vitro Proceedings of the National Academy of Sciences of the United States of America High 9207062
1998 The deoxyribose phosphate (dRP) lyase and AP lyase activities of pol β were characterized kinetically. The 8-kDa N-terminal domain of pol β is sufficient for both lyase activities. Km values are similar for dRP and AP lyase reactions, but kcat for AP lyase on an intact AP site is ~200-fold lower than on an AP endonuclease-preincised site. Mg2+ is not required for dRP lyase activity. Pyridoxal 5'-phosphate inhibits dRP lyase, consistent with Lys72 acting as a Schiff base nucleophile in the lyase mechanism. Steady-state kinetics with purified full-length pol β and isolated 8-kDa domain; pyridoxal 5'-phosphate inhibition assay; Mg2+ omission experiments The Journal of biological chemistry High 9614142
2001 XRCC1 interacts with human polynucleotide kinase (PNK) in addition to pol β and DNA ligase III, and these four proteins co-associate in multiprotein complexes in human cell extract. XRCC1 stimulates both the DNA kinase and DNA phosphatase activities of PNK at damaged DNA termini, accelerating single-strand break repair initiated by reactive oxygen species or ionizing radiation. Co-immunoprecipitation from human cell extracts, in vitro kinase/phosphatase assays, reconstituted repair assay Cell High 11163244
2004 NEIL1 DNA glycosylase stably interacts with pol β and DNA ligase IIIα to form a complex. This complex, together with PNK, defines an AP endonuclease-independent BER pathway for oxidized base lesions generating 3'-phosphate termini, where PNK (not APE1) removes 3'-phosphate blocking groups, and pol β performs gap-filling synthesis. Co-immunoprecipitation (stable complex formation), reconstituted repair assay with purified proteins, genetic complementation Molecular cell High 15260972
2013 Real-time crystallography of pol β with natural (non-analog) substrates captured 15 distinct structural intermediates during correct and incorrect nucleotide insertion. A transient third metal binding site forms during correct but not incorrect nucleotide insertion, promoting catalytic activation. Pyrophosphate dissociates more readily after incorrect insertion, coupled to subdomain repositioning required for catalytic deactivation. These findings reveal molecular determinants of polymerase fidelity at the active site. Real-time X-ray crystallography with natural substrates (correct and incorrect nucleotides), 15 crystal structures Cell High 23827680
2012 Sequencing of 134 human colorectal tumors revealed POLB coding mutations in 40% of samples. A subset of tumor-derived pol β variants showed reduced polymerase activity in vitro and failed to rescue pol β-deficient cells from methylmethane sulfonate (MMS)-induced cytotoxicity, indicating compromised BER function. These variants were scattered across the protein and not clustered, suggesting diverse mechanisms of functional disruption. POLB gene sequencing of tumor samples, in vitro enzymatic activity assays, MMS cytotoxicity rescue assays in pol β-deficient cells The Journal of biological chemistry Medium 22577134
2014 A hypomorphic mouse POLB allele encoding a pol β protein with slow polymerase activity (Y265C) leads to an autoimmune pathology strongly resembling systemic lupus erythematosus (SLE), with shorter immunoglobulin heavy-chain junctions and dramatically increased somatic hypermutation. This demonstrates that decreased pol β activity during immune diversity generation drives lupus-like disease, linking BER fidelity to autoimmunity. Mouse knockin model (POLB-Y265C hypomorphic allele), immunological and histopathological analysis, antibody repertoire sequencing Cell reports High 24388753
2017 Two independent groups reported that pol β (POLB), previously considered exclusively a nuclear BER enzyme, localizes to mitochondria and plays a significant role in mitochondrial base excision repair (mtBER), mtDNA integrity, and mitochondrial function. Subcellular fractionation, mitochondrial localization assays, functional mtDNA integrity assays (as described in commentary reviewing two primary studies) DNA repair Medium 29129598
2021 The Pol β-Y265C protein exhibits low catalytic activity, low fidelity, and is deficient in microhomology-mediated end-joining. PolbY265C/+ and PolbY265C/C mice accumulate BER intermediates leading to cell death; debris from dying cells drives lupus development. Deletion of upstream DNA glycosylases Neil1 and Ogg1 reduced BER intermediate accumulation and ameliorated renal disease severity in these mice, establishing epistatic placement of pol β downstream of these glycosylases in BER. Genetic epistasis (double-knockout mouse models), antinuclear antibody assays, renal histopathology, IgM measurement DNA repair High 34186496
2022 Bone marrow transplantation experiments demonstrated that the hematopoietic compartment from POLBY265C/C mice is sufficient to cause lupus-like disease (high antinuclear antibodies, renal disease) in wild-type congenic recipients, establishing that the aberrant immune repertoire generated by defective pol β activity in hematopoietic cells is the proximate driver of autoimmune pathology. Bone marrow transplantation into congenic wild-type mice, antinuclear antibody assays, renal pathology PloS one Medium 35486639
2025 CRISPR screens identified POLB as a synthetic lethal enhancer of PARP inhibition specifically in BRCA1/2-mutated cancers. POLB knockout combined with PARPi increased DNA single- and double-strand breaks, cell-cycle arrest, and apoptosis selectively in BRCA1/2-mutant cells. Overexpression of both wild-type and catalytically inactive POLB mutants confirmed that perturbation of both the polymerase and lyase catalytic activities of POLB are required for the synthetic lethal interaction. In murine xenograft models, POLB KO plus niraparib caused profound tumor regression. CRISPR screens, POLB knockout and overexpression (wild-type and catalytic mutants), DNA damage assays, cell viability assays, murine xenograft models Molecular cancer therapeutics High 40326293
2024 A high-throughput duplexed SAMDI mass spectrometry assay confirmed that POLB possesses two distinct enzymatic activities—lyase and polymerase—that can be simultaneously measured. Screening of 200,000 small molecules identified inhibitors of each activity; KO and rescue studies in BRCA1/2-mutant cells confirmed that inhibition of both lyase and polymerase activities is required for the synthetic lethal interaction with PARP inhibitors. SAMDI mass spectrometry-based high-throughput dual-activity assay, fluorescence-based polymerase strand-displacement assay, ASMS affinity selection, BRCA1/2-mutant cell rescue studies SLAS technology Medium 39094983
1986 The human DNA polymerase beta gene (POLB) was mapped to chromosome 8 by Southern blot hybridization analysis of a panel of human-mouse somatic cell hybrid DNAs using a rat pol β cDNA probe. Southern blot hybridization of somatic cell hybrid DNA panel Japanese journal of cancer research : Gann Medium 3009375

Source papers

Stage 0 corpus · 69 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
2013 Lenalidomide causes selective degradation of IKZF1 and IKZF3 in multiple myeloma cells. Science (New York, N.Y.) 1480 24292625
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
1996 Reconstitution of DNA base excision-repair with purified human proteins: interaction between DNA polymerase beta and the XRCC1 protein. The EMBO journal 644 8978692
1997 Crystal structures of human DNA polymerase beta complexed with gapped and nicked DNA: evidence for an induced fit mechanism. Biochemistry 561 9287163
2001 XRCC1 stimulates human polynucleotide kinase activity at damaged DNA termini and accelerates DNA single-strand break repair. Cell 506 11163244
1994 Oligo-capping: a simple method to replace the cap structure of eukaryotic mRNAs with oligoribonucleotides. Gene 492 8125298
2015 Widespread macromolecular interaction perturbations in human genetic disorders. Cell 454 25910212
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2004 AP endonuclease-independent DNA base excision repair in human cells. Molecular cell 403 15260972
1996 Normalization and subtraction: two approaches to facilitate gene discovery. Genome research 401 8889548
2005 Polymorphisms of DNA repair genes and risk of non-small cell lung cancer. Carcinogenesis 333 16195237
1997 Interaction of human apurinic endonuclease and DNA polymerase beta in the base excision repair pathway. Proceedings of the National Academy of Sciences of the United States of America 312 9207062
2010 Three DNA polymerases, recruited by different mechanisms, carry out NER repair synthesis in human cells. Molecular cell 310 20227374
1996 Crystal structures of human DNA polymerase beta complexed with DNA: implications for catalytic mechanism, processivity, and fidelity. Biochemistry 257 8841118
2014 Proximity biotinylation and affinity purification are complementary approaches for the interactome mapping of chromatin-associated protein complexes. Journal of proteomics 215 25281560
2006 Polymorphisms in genes of nucleotide and base excision repair: risk and prognosis of colorectal cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 209 16609022
2013 Observing a DNA polymerase choose right from wrong. Cell 192 23827680
2013 The protein interaction landscape of the human CMGC kinase group. Cell reports 174 23602568
1998 Human DNA polymerase beta deoxyribose phosphate lyase. Substrate specificity and catalytic mechanism. The Journal of biological chemistry 169 9614142
2019 Genetic Screens Reveal FEN1 and APEX2 as BRCA2 Synthetic Lethal Targets. Molecular cell 167 30686591
2004 XRCC1 co-localizes and physically interacts with PCNA. Nucleic acids research 163 15107487
2019 H4K20me0 recognition by BRCA1-BARD1 directs homologous recombination to sister chromatids. Nature cell biology 162 30804502
1999 DNA polymerase II (polB) is involved in a new DNA repair pathway for DNA interstrand cross-links in Escherichia coli. Journal of bacteriology 100 10217781
2012 Human POLB gene is mutated in high percentage of colorectal tumors. The Journal of biological chemistry 88 22577134
1990 The Escherichia coli polB gene, which encodes DNA polymerase II, is regulated by the SOS system. Journal of bacteriology 85 2228959
1992 Isolation of DNA damage-inducible promoters in Escherichia coli: regulation of polB (dinA), dinG, and dinH by LexA repressor. Journal of bacteriology 78 1577702
1997 The Escherichia coli polB locus is identical to dinA, the structural gene for DNA polymerase II. Characterization of Pol II purified from a polB mutant. The Journal of biological chemistry 62 9079692
2014 Mutation of POLB causes lupus in mice. Cell reports 48 24388753
2017 POLB: A new role of DNA polymerase beta in mitochondrial base excision repair. DNA repair 34 29129598
1991 Recurrent homogeneously staining regions in 8p1 in breast cancer and lack of amplification of POLB, LHRH, and PLAT genes. Cancer genetics and cytogenetics 29 1706959
1997 Mutation analysis of 8p genes POLB and PPP2CB in bladder cancer. Cancer genetics and cytogenetics 27 9078303
1989 Cloning the polB gene of Escherichia coli and identification of its product. The Journal of biological chemistry 24 2684981
1995 Functional recA, lexA, umuD, umuC, polA, and polB genes are not required for the Escherichia coli UVM response. Journal of bacteriology 23 7592365
2015 Clinical significance of a point mutation in DNA polymerase beta (POLB) gene in gastric cancer. International journal of biological sciences 21 25561897
2009 Population-specific variation in haplotype composition and heterozygosity at the POLB locus. DNA repair 19 19167932
2011 In vivo characterization of the homing endonuclease within the polB gene in the halophilic archaeon Haloferax volcanii. PloS one 18 21283796
1990 Nucleotide sequence and deletion analysis of the polB gene of Escherichia coli. DNA and cell biology 18 2261080
2016 Secondary Interaction Interfaces with PCNA Control Conformational Switching of DNA Polymerase PolB from Polymerization to Editing. The journal of physical chemistry. B 16 27109703
2009 Genetic insertions and diversification of the PolB-type DNA polymerase (gp43) of T4-related phages. Journal of molecular biology 14 19896487
2004 Molecular evolution of a mitochondrial polB gene, encoding a family B DNA polymerase, towards the elimination from Agrocybe mitochondrial genomes. Molecular genetics and genomics : MGG 14 15365817
1999 Molecular cloning, sequence and expression of Aa-polB, a mitochondrial gene encoding a family B DNA polymerase from the edible basidiomycete Agrocybe aegerita. Molecular & general genetics : MGG 13 10323231
1986 Assignment of the gene for human DNA polymerase beta (POLB) to chromosome 8. Japanese journal of cancer research : Gann 13 3009375
2016 A Point Mutation in DNA Polymerase β (POLB) Gene Is Associated with Increased Progesterone Receptor (PR) Expression and Intraperitoneal Metastasis in Gastric Cancer. Journal of Cancer 11 27471563
2014 Involvement of stress-related genes polB and PA14_46880 in biofilm formation of Pseudomonas aeruginosa. Infection and immunity 8 25156741
2015 Genetic Variants of IκB Kinase β (IKBKB) and Polymerase β (POLB) Were Not Associated with Systemic Lupus Erythematosus Risk in a Chinese Han Population. PloS one 7 26167925
2001 Duplication of a truncated paralog of the family B DNA polymerase gene Aa-polB in the Agrocybe aegerita mitochondrial genome. Applied and environmental microbiology 7 11282628
2020 Protein Splicing Activity of the Haloferax volcanii PolB-c Intein Is Sensitive to Homing Endonuclease Domain Mutations. Biochemistry 6 32822531
2016 Association Study of a Proliferation-inducing Ligand, Spermatogenesis Associated 8, Platelet-derived Growth Factor Receptor-alpha, and POLB Polymorphisms with Systemic Lupus Erythematosus in Chinese Han Population. Chinese medical journal 6 27569236
2014 Synergistic template-free synthesis of dsDNA by Thermococcus nautili primase PolpTN2, DNA polymerase PolB, and pTN2 helicase. Extremophiles : life under extreme conditions 6 25420601
2021 DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model. DNA repair 5 34186496
2025 CRISPR Screens Identify POLB as a Synthetic Lethal Enhancer of PARP Inhibition Exclusively in BRCA-Mutated Tumors. Molecular cancer therapeutics 3 40326293
2024 Analysis of Cancer-Associated Mutations of POLB Using Machine Learning and Bioinformatics. IEEE/ACM transactions on computational biology and bioinformatics 3 38691429
2024 A duplexed high-throughput mass spectrometry assay for bifunctional POLB polymerase and lyase activity. SLAS technology 3 39094983
2022 Polymorphic mutations in the polb gene promoter and their impact on transcriptional activity. Thoracic cancer 3 35128818
2022 The hematopoietic compartment is sufficient for lupus development resulting from the POLB-Y265C mutation. PloS one 1 35486639
2020 DNA alternate polymerase PolB mediates inhibition of type III secretion in Pseudomonas aeruginosa. Microbes and infection 1 33276123
2026 Genomic profiling of active vitamin D colonic responses in African- and European-Americans identifies an ancestry-related regulatory variant of POLB. PLoS genetics 0 41505470
2026 POLB 001, a p38 MAPK inhibitor, decreases local and systemic inflammatory responses following in vivo LPS administration in healthy volunteers: a randomised, double-blind, placebo-controlled study. Frontiers in immunology 0 41660627
2025 Endogenized polinton-like viruses in the dinoflagellate Oxyrrhis marina uncover novel PolB fusion. The Journal of general virology 0 41427953
2024 POLB Regulates Proliferation and Apoptosis of Bovine Primary Myocytes. Animals : an open access journal from MDPI 0 38731327
1982 [Effect of polB mutation on the nature of the thymineless death of thy- cells of Escherichia coli K-12]. Genetika 0 6754528