Affinage

POLE

DNA polymerase epsilon catalytic subunit A · UniProt Q07864

Length
2286 aa
Mass
261.5 kDa
Annotated
2026-04-28
100 papers in source corpus 13 papers cited in narrative 13 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

POLE encodes the catalytic subunit of DNA polymerase epsilon, which carries out leading-strand DNA replication and harbors an intrinsic 3'→5' exonuclease domain that proofreads mispaired bases during synthesis. Germline or somatic missense mutations in the exonuclease domain—such as p.Leu424Val, P286R, and V411L—abolish proofreading activity, producing microsatellite-stable, ultramutated tumors (>100 mut/Mb) with a characteristic mutational signature enriched for C>A and T>G transversions; the specific mutant allele, its expression level, and concurrent mismatch repair status determine the exact mutational spectrum and burden (PMID:23263490, PMID:32497495, PMID:31829442, PMID:25394778). The resulting high neoantigen load, including neoantigens with increased hydrophobicity at TCR-contact residues, drives robust CD4+ T cell responses and enhanced sensitivity to immune checkpoint blockade (PMID:25931171, PMID:35817971). Homozygous loss-of-function of POLE causes a chromosome instability syndrome with growth retardation, microcephaly, immune deficiency, and myelodysplasia (PMID:25948378).

Mechanistic history

Synthesis pass · year-by-year structured walk · 8 steps
  1. 2012 High

    Establishing that germline POLE exonuclease domain mutations (p.Leu424Val) cause loss of proofreading during replication answered the foundational question of how proofreading polymerase defects drive base-substitution hypermutation without microsatellite instability.

    Evidence Whole-genome sequencing of familial colorectal cancer kindreds plus yeast functional assays confirming exonuclease activity loss

    PMID:23263490

    Open questions at the time
    • Mechanism by which specific residue substitutions differentially affect polymerase fidelity was not resolved
    • Spectrum of pathogenic versus non-pathogenic POLE variants not yet delineated
    • Contribution of MMR as a secondary correction mechanism not quantified
  2. 2014 High

    Systematic molecular characterization of endometrial carcinomas showed that somatic POLE exonuclease domain mutations (P286R, V411L) define an ultramutated tumor subtype mechanistically distinct from MMR-deficient tumors, establishing POLE proofreading defects as an independent driver of hypermutation in sporadic cancer.

    Evidence Sanger sequencing plus TCGA whole-exome data with microsatellite stability testing in endometrial carcinoma cohorts

    PMID:25394778

    Open questions at the time
    • No direct enzymatic measurement of polymerase fidelity for the somatic mutants in human cells
    • Cooperative role of co-mutated genes (PTEN, PIK3CA) not mechanistically tested
  3. 2015 Medium

    Demonstrating that POLE-ultramutated tumors generate high neoantigen loads eliciting robust CD4+ Th1 immune responses linked POLE proofreading deficiency to tumor immunogenicity, answering why these hypermutated cancers paradoxically have favorable outcomes.

    Evidence Autologous dendritic cell stimulation, CFSE proliferation, 51Cr cytotoxicity, and intracellular cytokine assays in POLE-mutant versus wild-type endometrial cancers

    PMID:25931171

    Open questions at the time
    • CD8+ cytotoxic responses and in vivo immune killing not directly measured
    • Contribution of specific neoantigens versus total burden not dissected
    • Single-lab study without independent replication
  4. 2015 Medium

    A homozygous POLE splice variant causing complete loss of function resulted in a chromosome instability syndrome with microcephaly, immune deficiency, and myelodysplasia, establishing that POLE is essential for normal human development beyond its cancer-proofreading role.

    Evidence Exome sequencing and clinical phenotyping of a single patient with homozygous POLE1 splice variant

    PMID:25948378

    Open questions at the time
    • Single patient; no complementation or rescue experiment performed
    • Whether the developmental phenotype reflects replication defects, DNA repair defects, or both is unresolved
    • Cellular mechanism of chromosome instability not characterized
  5. 2015 Medium

    Epistasis analysis showed that when POLE exonuclease domain mutations co-occur with MMR deficiency, the POLE mutational signature dominates, establishing the hierarchical relationship between these two DNA fidelity mechanisms.

    Evidence Exome sequencing, MMR protein IHC, MSI analysis, and mutational signature comparison in doubly-deficient tumors

    PMID:26648449

    Open questions at the time
    • Mechanism of dominance (e.g., error rate versus error type) not dissected biochemically
    • Limited sample size of concurrent POLE/MMR-deficient cases
  6. 2020 High

    CRISPR-engineered human cells expressing specific POLE tumor variants revealed that different mutant alleles produce distinct mutational signatures even with intact MMR, resolving the question of whether allele identity or MMR status is the primary determinant of mutational spectrum.

    Evidence CRISPR-Cas9 knock-in of POLE variants in human cell lines with/without MMR, whole-exome sequencing after defined population doublings

    PMID:32497495

    Open questions at the time
    • Biochemical basis for allele-specific signature differences (e.g., altered base selectivity) not determined
    • Long-term fitness consequences of different POLE alleles not assessed
  7. 2020 High

    Development of the POLE-score system using signature-based genomic criteria (C>A >20%, T>G >4%, TMB >100 mut/Mb) distinguished pathogenic from non-pathogenic POLE variants, answering the variant-interpretation problem that had accumulated since the initial discovery.

    Evidence Systematic whole-exome sequencing analysis of TCGA endometrial carcinomas with mutational signature quantification

    PMID:31829442

    Open questions at the time
    • POLE-score validated only in endometrial cancer; applicability to other tumor types not established
    • No direct enzymatic assay validation of scored variants
  8. 2022 High

    Mechanistic characterization of POLE/POLD1-driven neoantigens revealed increased hydrophobicity at TCR-contact residues, explaining enhanced T cell recognition and providing a biochemical basis for the exceptional immune checkpoint blockade response seen in POLE-mutant tumors.

    Evidence Murine syngeneic tumor models with Pole mutations, neoantigen biochemical property analysis, patient ICB response correlation

    PMID:35817971

    Open questions at the time
    • Whether hydrophobicity-driven immunogenicity generalizes beyond the tested neoantigen repertoire is unclear
    • Relative contribution of POLE versus POLD1 neoantigens to immunogenicity not separated
    • No structural data on TCR–neoantigen interactions

Open questions

Synthesis pass · forward-looking unresolved questions
  • The structural and biochemical basis by which individual POLE exonuclease domain substitutions differentially alter nucleotide selectivity and fidelity—and how the resulting mutational processes interact with chromatin context and replication timing—remains unresolved.
  • No high-resolution structure of human POLE holoenzyme with mutant exonuclease domain
  • Allele-specific differences in polymerase kinetics not measured in vitro with purified human enzyme
  • Relationship between replication timing, chromatin state, and POLE-driven mutagenesis not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140097 catalytic activity, acting on DNA 3 GO:0003677 DNA binding 2
Localization
GO:0005634 nucleus 3
Pathway
R-HSA-1643685 Disease 4 R-HSA-69306 DNA Replication 4 R-HSA-168256 Immune System 2 R-HSA-73894 DNA Repair 2
Partners
POLD1PTEN
Complex memberships
DNA polymerase epsilon

Evidence

Reading pass · 13 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 Germline mutations in the proofreading (exonuclease) domain of POLE (p.Leu424Val) cause defects in correction of mispaired bases inserted during DNA replication, leading to base substitution hypermutation in tumors while remaining microsatellite stable. Yeast functional assays confirmed loss of exonuclease proofreading activity. Whole-genome sequencing, linkage/association analysis, yeast functional assays for exonuclease activity Nature genetics High 23263490
2020 POLE exonuclease domain mutations (EDMs) cause loss of proofreading function, generating a characteristic mutational signature including >20% C>A substitutions, >4% T>G substitutions, <0.6% C>G substitutions, and tumor mutational burden >100 mut/Mb. A scoring system (POLE-score) based on these genomic alterations distinguishes pathogenic from non-pathogenic POLE mutations. Mutations outside the exonuclease domain are predominantly not pathogenic. Whole-exome sequencing of TCGA endometrial carcinomas, mutational signature analysis, POLE-score development The Journal of pathology High 31829442
2020 POLE cancer mutant alleles drive characteristic mutational signature accumulation even in the presence of functional mismatch repair (MMR), unlike an exonuclease active-site mutant. The relative abundance of mutation signatures partitions POLE tumors into distinct subgroups dependent on the specific POLE allele, its expression level, and MMR status, revealing that different POLE mutants have distinct effects on replication fidelity. CRISPR-Cas9 engineering of human cell lines expressing POLE tumor variants with/without MMR, whole-exome sequencing after defined population doublings Molecular cell High 32497495
2019 POLE proofreading-deficient tumors accumulate extensive somatic mutations via loss of exonuclease proofreading activity during DNA replication. The proofreading domain of POLE corrects mispaired bases; mutations in this domain allow errors to persist, leading to hypermutation. MMR further modulates the mutational spectrum. Cancer genome sequencing, mutational signature analysis, review of yeast and mouse model data DNA repair High 30818169
2015 A novel POLE mutation (p.Tyr458Phe) located in the active site of the exonuclease domain affects a residue previously shown to be important for exonuclease activity, expanding the tumor spectrum of POLE mutation carriers to include cancers of colon, pancreas, ovaries, and small intestine. Exome sequencing, pedigree analysis, identification of active-site residue involved in exonuclease catalysis Familial cancer Medium 25860647
2014 The POLE mutation p.Asn363Lys (c.1089C>A) is located in the proofreading exonuclease domain at a residue directly involved in DNA binding, predicted to profoundly affect substrate binding capability and catalytic activity of the exonuclease, leading to a broader tumor spectrum than p.Leu424Val. Sequencing, in silico structural prediction of amino acid substitution effect on DNA binding International journal of oncology Medium 24788313
2015 POLE exonuclease domain mutations generate ultra-mutated tumors with a high neoantigen load, inducing robust tumor-specific CD4+ T cell responses and a Th1 cytokine bias (IFN-γ), and significantly more immunogenic responses compared to POLE wild-type endometrial cancers. Autologous dendritic cell stimulation assay, CFSE proliferation assay, [3H]-thymidine incorporation, 51Cr cytotoxicity assay, intracellular cytokine flow cytometry Gynecologic oncology Medium 25931171
2017 A POLE variant (c.1420G>A, p.Val474Ile) located adjacent to the exonuclease domain was shown by functional assays in Schizosaccharomyces pombe to impair proofreading activity, representing the first functional analysis of a POLE variant outside the canonical exonuclease domain. Sanger sequencing, bioinformatics prediction, S. pombe functional assay for proofreading activity Oncotarget Medium 28423643
2022 Pathogenic POLE/POLD1 mutations that cause functional proofreading deficiency generate specific mutational signatures and produce neoantigens with increased hydrophobicity at TCR-contact residues, facilitating T cell recognition and enhancing immune checkpoint blockade response. Murine syngeneic tumors with Pole/Pold1 functional mutations displayed enhanced antitumor immunity sensitive to ICB. Murine syngeneic tumor models, mutational signature analysis, biochemical analysis of neoantigen properties, patient ICB response correlation Nature genetics High 35817971
2019 Defective POLE proofreading leads to extensive somatic mutation accumulation following a temporally ordered pattern: mutations in cancer-related genes occur before the aberrant POLE event, PTEN mutations co-occur with or follow POLE mutations, and homologous recombination is restored after PTEN mutation, suggesting POLE and PTEN cooperate in tumorigenic development. Whole-exome sequencing of 10 POLE-mutated solid tumors, sequential mutation shift analysis Scientific reports Medium 29880869
2015 POLE exonuclease domain mutations co-occurring with MMR deficiency/MSI-H produce genomic alterations characteristic of POLE-ultramutated tumors, indicating that the POLE proofreading defect is dominant over MMR deficiency in determining the mutational phenotype when both are present. Exome sequencing, MMR protein IHC, MSI analysis, mutational signature analysis in combined MMR-deficient/POLE-mutated tumors European journal of human genetics Medium 26648449
2015 A patient with homozygous POLE1 (catalytic subunit of DNA polymerase epsilon) splice variant (c.4444+3A>G) presented with growth retardation, microcephaly, developmental delay, immune deficiency with pancytopenia, and myelodysplasia, demonstrating that complete loss of POLE1 function causes a chromosome instability syndrome in humans. Exome sequencing, clinical phenotyping BMC medical genetics Medium 25948378
2014 POLE somatic exonuclease domain mutations (including P286R, V411L) define an ultramutated endometrial carcinoma subtype characterized by microsatellite stability, high tumor mutation rate, and distinct co-mutations in PTEN, FBXW7, ARID1A, and PIK3CA, establishing POLE proofreading defects as a driver of hypermutation distinct from MMR deficiency. Sanger sequencing of POLE exonuclease domain, TCGA whole-exome sequencing data analysis, microsatellite stability testing Modern pathology High 25394778

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Germline mutations affecting the proofreading domains of POLE and POLD1 predispose to colorectal adenomas and carcinomas. Nature genetics 770 23263490
1999 Rapid pole-to-pole oscillation of a protein required for directing division to the middle of Escherichia coli. Proceedings of the National Academy of Sciences of the United States of America 568 10220403
1990 Posterior localization of vasa protein correlates with, but is not sufficient for, pole cell development. Genes & development 345 2384213
2020 Interpretation of somatic POLE mutations in endometrial carcinoma. The Journal of pathology 323 31829442
2016 Immune activation and response to pembrolizumab in POLE-mutant endometrial cancer. The Journal of clinical investigation 315 27159395
2001 Aubergine encodes a Drosophila polar granule component required for pole cell formation and related to eIF2C. Development (Cambridge, England) 275 11526087
2001 Pattern formation in Escherichia coli: a model for the pole-to-pole oscillations of Min proteins and the localization of the division site. Proceedings of the National Academy of Sciences of the United States of America 268 11734639
2008 A polymeric protein anchors the chromosomal origin/ParB complex at a bacterial cell pole. Cell 256 18805088
2004 The budding yeast spindle pole body: structure, duplication, and function. Annual review of cell and developmental biology 231 15473833
2010 WDR62 is associated with the spindle pole and is mutated in human microcephaly. Nature genetics 228 20890279
2000 The molecular motor dynein is involved in targeting swallow and bicoid RNA to the anterior pole of Drosophila oocytes. Nature cell biology 207 10783235
2002 The anterior heart-forming field: voyage to the arterial pole of the heart. Trends in genetics : TIG 193 11932022
2012 Pole-to-pole biogeography of surface and deep marine bacterial communities. Proceedings of the National Academy of Sciences of the United States of America 192 23045668
2013 Cytoarchitecture, probability maps and functions of the human frontal pole. NeuroImage 183 23702412
2014 Clinicopathological analysis of endometrial carcinomas harboring somatic POLE exonuclease domain mutations. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 163 25394778
1999 Sid2p, a spindle pole body kinase that regulates the onset of cytokinesis. The Journal of cell biology 159 10459013
1989 Centrosomes, and not nuclei, initiate pole cell formation in Drosophila embryos. Cell 155 2497990
2003 RHAMM is a centrosomal protein that interacts with dynein and maintains spindle pole stability. Molecular biology of the cell 149 12808028
2014 Polymerase ɛ (POLE) mutations in endometrial cancer: clinical outcomes and implications for Lynch syndrome testing. Cancer 144 25224212
2013 How do bacteria localize proteins to the cell pole? Journal of cell science 144 24345373
2000 Bacterial activity in South Pole snow. Applied and environmental microbiology 143 11010907
2012 A multidomain hub anchors the chromosome segregation and chemotactic machinery to the bacterial pole. Genes & development 138 23070816
2014 New insights into POLE and POLD1 germline mutations in familial colorectal cancer and polyposis. Human molecular genetics 123 24501277
2022 Mechanism of spindle pole organization and instability in human oocytes. Science (New York, N.Y.) 115 35143306
2015 Combined mismatch repair and POLE/POLD1 defects explain unresolved suspected Lynch syndrome cancers. European journal of human genetics : EJHG 107 26648449
2013 Aurora at the pole and equator: overlapping functions of Aurora kinases in the mitotic spindle. Open biology 100 23516109
2010 CDK5RAP2 functions in centrosome to spindle pole attachment and DNA damage response. The Journal of cell biology 100 20368616
2020 Role of POLE and POLD1 in familial cancer. Genetics in medicine : official journal of the American College of Medical Genetics 99 32792570
2015 Aurora A Kinase Contributes to a Pole-Based Error Correction Pathway. Current biology : CB 98 26166783
2005 Regulated pole-to-pole oscillations of a bacterial gliding motility protein. Science (New York, N.Y.) 97 16272122
2018 Peptidoglycan precursor synthesis along the sidewall of pole-growing mycobacteria. eLife 96 30198841
2022 POLE/POLD1 mutation and tumor immunotherapy. Journal of experimental & clinical cancer research : CR 91 35780178
1995 Cell adhesion to the apical pole of epithelium: a function of cell polarity. European journal of cell biology 90 7774604
2004 Drosophila tudor is essential for polar granule assembly and pole cell specification, but not for posterior patterning. Genesis (New York, N.Y. : 2000) 86 15495201
2014 Bacterial scaffold directs pole-specific centromere segregation. Proceedings of the National Academy of Sciences of the United States of America 85 24778223
2006 Inhibitors of Polo-like kinase reveal roles in spindle-pole maintenance. Nature chemical biology 85 17028581
2018 Macropinosome formation by tent pole ruffling in macrophages. The Journal of cell biology 81 30150290
2001 Asymmetric spindle pole localization of yeast Cdc15 kinase links mitotic exit and cytokinesis. Current biology : CB 79 11267871
2011 Biogenesis of the posterior pole is mediated by the exosome/microvesicle protein-sorting pathway. The Journal of biological chemistry 77 21865156
2002 The distal pole complex: a novel membrane domain distal to the immunological synapse. Immunological reviews 74 12445269
2015 From equator to pole: splitting chromosomes in mitosis and meiosis. Genes & development 70 25593304
2014 zic-1 Expression in Planarian neoblasts after injury controls anterior pole regeneration. PLoS genetics 70 24992682
2010 Arterial pole progenitors interpret opposing FGF/BMP signals to proliferate or differentiate. Development (Cambridge, England) 70 20702561
2015 A novel POLE mutation associated with cancers of colon, pancreas, ovaries and small intestine. Familial cancer 66 25860647
2005 Caulobacter crescentus requires RodA and MreB for stalk synthesis and prevention of ectopic pole formation. Journal of bacteriology 65 15629926
2019 Phenotype of POLE-mutated endometrial cancer. PloS one 64 30917185
2015 Polymerase ε (POLE) ultra-mutated tumors induce robust tumor-specific CD4+ T cell responses in endometrial cancer patients. Gynecologic oncology 64 25931171
2011 Identification of a Tbx1/Tbx2/Tbx3 genetic pathway governing pharyngeal and arterial pole morphogenesis. Human molecular genetics 61 22116936
2022 Functional landscapes of POLE and POLD1 mutations in checkpoint blockade-dependent antitumor immunity. Nature genetics 60 35817971
2014 A mutation in POLE predisposing to a multi-tumour phenotype. International journal of oncology 59 24788313
2020 POLE Mutation Spectra Are Shaped by the Mutant Allele Identity, Its Abundance, and Mismatch Repair Status. Molecular cell 58 32497495
2016 Polymerase ε (POLE) ultra-mutation in uterine tumors correlates with T lymphocyte infiltration and increased resistance to platinum-based chemotherapy in vitro. Gynecologic oncology 58 27894751
1997 The yeast CDC37 gene interacts with MPS1 and is required for proper execution of spindle pole body duplication. The Journal of cell biology 57 9060463
2024 Immune checkpoint inhibitors for POLE or POLD1 proofreading-deficient metastatic colorectal cancer. Annals of oncology : official journal of the European Society for Medical Oncology 55 38777726
2003 The chromokinesin, KLP3A, dives mitotic spindle pole separation during prometaphase and anaphase and facilitates chromatid motility. Molecular biology of the cell 55 14528012
2019 Clinical outcomes of patients with POLE mutated endometrioid endometrial cancer. Gynecologic oncology 54 31757464
2008 Aurora-A and ch-TOG act in a common pathway in control of spindle pole integrity. Oncogene 52 18663358
2019 POLE proofreading defects: Contributions to mutagenesis and cancer. DNA repair 50 30818169
2005 The type IV secretion apparatus protein VirB6 of Agrobacterium tumefaciens localizes to a cell pole. Molecular microbiology 50 15612921
2003 A lytic transglycosylase homologue, PleA, is required for the assembly of pili and the flagellum at the Caulobacter crescentus cell pole. Molecular microbiology 50 12828633
2014 Lessons from yeast: the spindle pole body and the centrosome. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 47 25047610
2013 pbx is required for pole and eye regeneration in planarians. Development (Cambridge, England) 45 23318641
2022 A root phloem pole cell atlas reveals common transcriptional states in protophloem-adjacent cells. Nature plants 44 35927456
2019 Comprehensive analysis of POLE and POLD1 Gene Variations identifies cancer patients potentially benefit from immunotherapy in Chinese population. Scientific reports 44 31673068
2017 POLE and POLD1 screening in 155 patients with multiple polyps and early-onset colorectal cancer. Oncotarget 43 28423643
2017 Risk of colorectal cancer for carriers of a germ-line mutation in POLE or POLD1. Genetics in medicine : official journal of the American College of Medical Genetics 43 29120461
2007 Mechanisms of spindle-pole organization are influenced by kinetochore activity in mammalian cells. Current biology : CB 42 17276919
2021 Distinct mutational profile and immune microenvironment in microsatellite-unstable and POLE-mutated tumors. Journal for immunotherapy of cancer 40 34607897
2022 Yeast osmoregulation - glycerol still in pole position. FEMS yeast research 39 35927716
2018 Clinicopathological characteristics of POLE mutation in patients with non-small-cell lung cancer. Lung cancer (Amsterdam, Netherlands) 39 29572003
2015 GREM1 and POLE variants in hereditary colorectal cancer syndromes. Genes, chromosomes & cancer 38 26493165
2021 Tumor-infiltrating lymphocytes and POLE mutation in endometrial carcinoma. Gynecologic oncology 36 33715893
2000 A spindle pole body-associated protein, SNAD, affects septation and conidiation in Aspergillus nidulans. Molecular & general genetics : MGG 36 10821171
2020 A biphasic growth model for cell pole elongation in mycobacteria. Nature communications 35 31974342
2015 PopZ identifies the new pole, and PodJ identifies the old pole during polar growth in Agrobacterium tumefaciens. Proceedings of the National Academy of Sciences of the United States of America 35 26324921
2021 The biogeographic differentiation of algal microbiomes in the upper ocean from pole to pole. Nature communications 34 34531387
1997 Expeditions to the pole: RNA localization in Xenopus and Drosophila. Trends in cell biology 34 17709012
2014 The KASH protein Kms2 coordinates mitotic remodeling of the spindle pole body. Journal of cell science 32 24963130
2018 Clinical impact of endometrial cancer stratified by genetic mutational profiles, POLE mutation, and microsatellite instability. PloS one 31 29659608
2004 nanos expression at the embryonic posterior pole and the medusa phase in the hydrozoan Podocoryne carnea. Evolution & development 31 15330869
2007 Dialogue between LKB1 and AMPK: a hot topic at the cellular pole. Science's STKE : signal transduction knowledge environment 30 17878409
2019 Clinicopathological and mutational analyses of colorectal cancer with mutations in the POLE gene. Cancer medicine 29 31240875
2016 Duplication of the Yeast Spindle Pole Body Once per Cell Cycle. Molecular and cellular biology 29 26951196
2014 Frequent POLE1 p.S297F mutation in Chinese patients with ovarian endometrioid carcinoma. Mutation research 29 24472300
2018 Nkx genes establish second heart field cardiomyocyte progenitors at the arterial pole and pattern the venous pole through Isl1 repression. Development (Cambridge, England) 28 29361575
2002 The Saccharomyces cerevisiae Fin1 protein forms cell cycle-specific filaments between spindle pole bodies. Proceedings of the National Academy of Sciences of the United States of America 28 11929974
2019 Germline POLE mutation in a child with hypermutated medulloblastoma and features of constitutional mismatch repair deficiency. Cold Spring Harbor molecular case studies 27 31624068
2017 Human microcephaly ASPM protein is a spindle pole-focusing factor that functions redundantly with CDK5RAP2. Journal of cell science 27 28883092
2015 A patient with polymerase E1 deficiency (POLE1): clinical features and overlap with DNA breakage/instability syndromes. BMC medical genetics 26 25948378
2024 Mechanisms of minor pole-mediated spindle bipolarization in human oocytes. Science (New York, N.Y.) 25 39172836
2018 Molecular profiling and sequential somatic mutation shift in hypermutator tumours harbouring POLE mutations. Scientific reports 25 29880869
2010 Targeting and anchoring Tudor in the pole plasm of the Drosophila oocyte. PloS one 25 21179512
2019 Morphological, immunophenotypical and molecular features of hypermutation in colorectal carcinomas with mutations in DNA polymerase ε (POLE). Histopathology 23 31479159
2020 Genomic Alterations of NTRK, POLE, ERBB2, and Microsatellite Instability Status in Chinese Patients with Colorectal Cancer. The oncologist 22 32627883
2019 Centromere Dysfunction Compromises Mitotic Spindle Pole Integrity. Current biology : CB 22 31495582
2019 Detection of POLE Subtypes in High-Grade Endometrioid Carcinoma by BaseScope-ISH Assay. Frontiers in oncology 21 31552169
2013 Automated tracking of mitotic spindle pole positions shows that LGN is required for spindle rotation but not orientation maintenance. Cell cycle (Georgetown, Tex.) 20 23907121
1992 From egg to pole cells: ultrastructural aspects of early cleavage and germ cell determination in insects. Microscopy research and technique 20 1617208
2020 CEP215 and AURKA regulate spindle pole focusing and aMTOC organization in mouse oocytes. Reproduction (Cambridge, England) 18 31895686
2022 Analysis of HubP-dependent cell pole protein targeting in Vibrio cholerae uncovers novel motility regulators. PLoS genetics 17 35020734