Affinage

ERCC6L

DNA excision repair protein ERCC-6-like · UniProt Q2NKX8

Length
1250 aa
Mass
141.1 kDa
Annotated
2026-04-28
52 papers in source corpus 26 papers cited in narrative 27 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ERCC6L (PICH) is a SNF2-family ATP-dependent DNA translocase essential for faithful chromosome segregation during mitosis. It binds duplex DNA with affinity that increases under mechanical tension, translocates along DNA in an ATP-dependent manner, remodels nucleosomes on stretched chromatin, and cooperates with BLM helicase and Topoisomerase IIα to resolve ultrafine anaphase DNA bridges (UFBs) formed by catenated or under-replicated sister chromatid DNA (PMID:23973328, PMID:36433994, PMID:21743438, PMID:26643143). PICH is recruited to centromeres and kinetochores through Cdk1-dependent phosphorylation that creates a Plk1-docking site, and its centromeric targeting further requires SUMO-interacting motifs that also mediate dispersal of SUMO2/3-modified chromosomal proteins including SUMOylated Topoisomerase IIα (PMID:17218258, PMID:27230136, PMID:32877270). Beyond mitosis, PICH participates in replication stress responses through the ZATT–TOP2A–PICH axis to promote fork reversal, and PICH knockout in mice causes embryonic lethality at E12.5 with chromosomal instability, cytoplasmic dsDNA accumulation, and cGAS–STING-driven innate immune activation that impairs fetal hematopoiesis (PMID:33296677, PMID:30232008, PMID:35037428).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2007 High

    The discovery that Cdk1 phosphorylation of PICH at T1063 recruits Plk1, directing PICH to centromeres and to previously unrecognized ultrafine DNA bridges in anaphase, established PICH as the first marker of UFBs and linked its localization to the mitotic kinase cascade.

    Evidence Co-IP, phosphorylation assays, mutagenesis, immunofluorescence, DNase sensitivity, and siRNA in human cells

    PMID:17218258

    Open questions at the time
    • Enzymatic activity of PICH on DNA had not been demonstrated
    • Whether PICH actively resolves UFBs or merely marks them was unknown
    • Initial SAC role attributed to PICH was subsequently shown to be an off-target siRNA artifact (PMID:19904549)
  2. 2008 Medium

    Showing that PICH targets Plk1 to chromosome arms and that PICH ATPase activity is needed for proper chromosome compaction established PICH as an active architectural regulator rather than a passive bridge marker, with Topoisomerase II functioning downstream.

    Evidence Co-IP, siRNA rescue with ATPase-dead and Plk1-binding-deficient mutants, immunofluorescence, ICRF-193 epistasis

    PMID:17956945 PMID:18418076 PMID:20130082

    Open questions at the time
    • Direct biochemical interaction between PICH and Topo IIα had not been reconstituted
    • How PICH ATPase activity influences chromosome architecture mechanistically was unclear
  3. 2011 High

    Demonstrating that PICH directly binds BLM, recruits it to UFBs, and possesses nucleosome remodeling activity in vitro revealed that PICH clears histones from anaphase bridges to enable downstream resolution enzymes.

    Evidence Co-IP, in vitro nucleosome remodeling with purified recombinant PICH, siRNA epistasis, immunofluorescence

    PMID:21743438

    Open questions at the time
    • Whether remodeling activity was tension-dependent was not tested
    • Contribution of PICH remodeling versus BLM helicase to UFB resolution was not separated
  4. 2013 High

    Single-molecule biophysics revealed that PICH binds DNA with affinity that increases under tension and translocates along DNA in an ATP-dependent manner, providing a mechanistic explanation for how PICH selectively recognizes stretched UFB DNA during anaphase.

    Evidence Optical tweezers, microfluidics, and fluorescence imaging with purified PICH protein

    PMID:23973328

    Open questions at the time
    • Behavior on chromatinized templates under tension had not been tested
    • In vivo validation of the tension-sensing model was lacking
  5. 2015 High

    Genetic knockout of PICH in avian and human cells combined with in vitro reconstitution showed that PICH directly stimulates Topoisomerase IIα catalytic activity, establishing a biochemical mechanism for how PICH promotes sister chromatid decatenation.

    Evidence PICH−/− DT40 and human cell lines, in vitro Topo II stimulation assay with purified proteins, ICRF-193 sensitivity

    PMID:26643143

    Open questions at the time
    • Whether stimulation depends on DNA topology (catenanes vs. supercoils) was not resolved
    • Structural basis of PICH–Topo IIα stimulation was not determined
  6. 2015 High

    Identifying PICH SUMOylation by PIASy and direct binding to SUMO-modified Topo IIα and PARP1 revealed SUMO as a key regulatory layer controlling PICH's DNA-binding capacity and its interaction with chromosomal substrates.

    Evidence Xenopus egg extracts, in vitro SUMOylation, purified-protein binding assays

    PMID:25564610

    Open questions at the time
    • Functional consequence of PICH SUMOylation in mammalian cells was not shown
    • Relative contributions of individual SIMs were not yet mapped
  7. 2016 Medium

    Mapping three SUMO-interacting motifs in PICH and showing distinct functional roles — SIM3 for centromeric targeting and SIM1/2 for chromatin bridge prevention — partitioned PICH's SUMO-dependent functions into separable activities.

    Evidence SIM-mutant rescue in conditionally depleted cells, immunofluorescence

    PMID:27230136

    Open questions at the time
    • Identity of the SIM1/2-targeted SUMOylated substrates was unknown
    • Whether SIMs regulate PICH's remodeling or translocase activity specifically was not tested
  8. 2017 High

    Solving the crystal structure of the PICH TPR domain bound to the BEND3 BEN domain at 2.2 Å identified a novel protein–protein interaction interface on PICH, expanding its interactome beyond known mitotic partners.

    Evidence X-ray crystallography, Co-IP, mutagenesis of interface residues

    PMID:28977671

    Open questions at the time
    • Functional role of the PICH–BEND3 interaction in mitosis was not established
    • Whether BEND3 modulates PICH translocase or remodeling activity was unknown
  9. 2018 High

    PICH knockout in mice causes embryonic lethality by E12.5 with widespread DNA damage, chromosomal instability, and p53-independent lethality, establishing PICH as essential for mammalian development and genome integrity in vivo.

    Evidence Pich-KO mouse, embryo phenotyping, p53 double-KO epistasis

    PMID:30232008

    Open questions at the time
    • Whether lethality is driven by mitotic or replication defects was not resolved
    • Tissue-specific requirements for PICH were unexplored
  10. 2019 High

    Reconstituting PICH with TOP3A in vitro revealed an unprecedented reverse-gyrase-like activity: PICH extrudes hypernegatively supercoiled loops that TOP3A relaxes to generate positive supercoiling, explaining how UFB DNA topology could be remodeled during anaphase.

    Evidence Single-molecule magnetic tweezers, fluorescence imaging with purified PICH and TOP3A

    PMID:30936532

    Open questions at the time
    • Whether positive supercoiling is generated in vivo on UFBs was not demonstrated
    • Relative contribution of positive supercoiling versus Topo IIα stimulation to UFB resolution was unclear
  11. 2020 High

    Discovery of the ZATT–TOP2A–PICH axis at stalled replication forks extended PICH's function beyond mitosis: SUMO-targeted recruitment of PICH by ZATT promotes extensive fork reversal, establishing a replication stress response role.

    Evidence iPOND, proximity ligation assay, replication fiber assay, electron microscopy of fork intermediates

    PMID:33296677

    Open questions at the time
    • Whether PICH's translocase activity directly drives branch migration at forks was not shown
    • Relationship between mitotic UFB function and fork reversal function was not dissected
  12. 2020 Medium

    Demonstrating that PICH disperses SUMO2/3-modified proteins from mitotic chromosomes in a translocase-dependent manner and attenuates SUMOylated Topo IIα activity established PICH as a SUMO-targeted chromatin remodeler with dual roles in activating and restraining Topo IIα.

    Evidence Auxin-inducible degron depletion, in vitro SUMOylated Topo IIα activity assay

    PMID:32877270

    Open questions at the time
    • In vivo consequences of impaired SUMO-protein dispersal on chromosome segregation fidelity were not quantified
    • Whether dispersal and stimulation of Topo IIα are temporally or spatially separated was unknown
  13. 2022 High

    Single-molecule assays on chromatinized templates under tension showed PICH facilitates nucleosome unwrapping and sliding in a tension- and ATP-dependent manner, directly confirming that PICH remodels chromatin on stretched anaphase bridges.

    Evidence Dual-trap optical tweezers with purified PICH and reconstituted nucleosome arrays

    PMID:36433994

    Open questions at the time
    • Whether other remodelers cooperate with PICH on UFB chromatin in vivo was not addressed
    • Histone fate after PICH-mediated unwrapping was not tracked
  14. 2022 High

    PICH-KO mouse embryos activate the cGAS–STING innate immune pathway due to cytoplasmic dsDNA, impairing fetal hematopoiesis — a phenotype rescued by Ifnar1 or cGAS deletion — revealing that chromosomal instability caused by PICH loss triggers autoinflammation.

    Evidence Pich-KO mouse, bone marrow transplantation, cGAS/Ifnar1 genetic rescue, flow cytometry

    PMID:35037428

    Open questions at the time
    • Source of cytoplasmic dsDNA (micronuclei, bridges, or replication intermediates) was not defined
    • Whether cGAS–STING activation occurs in PICH-depleted adult tissues was not tested
  15. 2023 Medium

    Genome-wide screens identified synthetic lethal relationships between PICH and FIRRM/FIGNL1 as well as compensatory roles with RAD52, placing PICH within a broader genetic network safeguarding genome integrity at replication intermediates and in mitosis.

    Evidence CRISPR knockout screens, siRNA epistasis, replication fork assays, immunofluorescence, UFB quantification

    PMID:37347663 PMID:39561207

    Open questions at the time
    • Biochemical mechanism of FIRRM/FIGNL1 dependency on PICH is unknown
    • Whether RAD52 and PICH act on the same DNA substrates was not shown
  16. 2025 Medium

    Dissecting PICH's translocase activity from its BLM-recruitment function showed that translocase activity is essential for both UFB resolution and chromosome condensation, while BLM/RIF1 recruitment plays a partial role; whole-genome sequencing revealed PICH loss causes structural chromosomal rearrangements.

    Evidence PICH separation-of-function mutants, siRNA rescue, whole-genome sequencing, immunofluorescence

    PMID:39704103

    Open questions at the time
    • Whether translocase-driven supercoiling or Topo IIα stimulation is the primary resolution mechanism in vivo remains unresolved
    • Structural basis of PICH translocase processivity is unknown
  17. 2025 Medium

    PICH was shown to influence the spindle assembly checkpoint through its remodeling activity and SUMO-binding: PICH defects cause prolonged SAC activation via extended Mad1 foci and altered Bub1 kinetochore association, revising an earlier discredited SAC connection.

    Evidence Conditional AID depletion, PICH mutant replacement, chromosomal SUMO proteomics, live-cell imaging

    PMID:39919802

    Open questions at the time
    • Whether PICH directly remodels kinetochore-proximal chromatin to control SAC signaling is not established
    • The SUMOylated substrate(s) whose dispersal affects Bub1 are not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions include the structural basis of PICH's tension-sensing translocase mechanism, the relative in vivo contributions of its positive supercoiling, Topo IIα stimulation, and nucleosome remodeling activities to UFB resolution, and whether its emerging transcriptional roles represent core or context-dependent functions.
  • No high-resolution structure of full-length PICH or PICH–DNA complex exists
  • In vivo separation of positive supercoiling, Topo IIα stimulation, and chromatin remodeling contributions has not been achieved
  • Transcriptional functions (Nrf2, CCNA1) require independent replication and mechanistic reconstitution

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 4 GO:0140657 ATP-dependent activity 4 GO:0140096 catalytic activity, acting on a protein 3 GO:0098772 molecular function regulator activity 2
Localization
GO:0005694 chromosome 5 GO:0005634 nucleus 3
Pathway
R-HSA-1640170 Cell Cycle 5 R-HSA-73894 DNA Repair 3 R-HSA-69306 DNA Replication 1
Partners
BEND3BLMFIRRMKIF4APLK1TOP2ATOP3AZATT
Complex memberships
PICH-BLMPICH-Plk1ZATT-TOP2A-PICH

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 PICH (ERCC6L) is phosphorylated by Cdk1 at T1063, which recruits Plk1 to PICH and controls its localization to kinetochores and inner centromeres during prometaphase. Co-immunoprecipitation, phosphorylation assays, site-directed mutagenesis, immunofluorescence Cell High 17218258
2007 PICH localizes to ultrafine DNA threads (UFBs) connecting sister kinetochores in anaphase; these threads are tension-dependent, DNase-sensitive, and exacerbated by cohesin loss or topoisomerase II inhibition, suggesting PICH binds catenated centromeric DNA. Immunofluorescence, DNase treatment, siRNA depletion, live-cell imaging Cell High 17218258
2007 Depletion of PICH causes selective loss of Mad2 from kinetochores and abrogates the spindle assembly checkpoint; however, subsequent work showed this effect was due to off-target siRNA reduction of Mad2 rather than a direct role of PICH in the checkpoint. siRNA depletion, immunofluorescence, Mad2-rescue BAC experiments Cell / Chromosoma High 17218258 19904549
2007 Depletion of topoisomerase IIα leads to abnormal persistence of PICH-coated anaphase threads, and shortens the metaphase interkinetochore distance, establishing a functional relationship between Topo IIα and PICH-coated UFBs. Conditional Topo IIα mutant cell line, immunofluorescence, FISH Journal of cell science Medium 17956945
2008 PICH targets Plk1 to chromosome arms during mitosis via a direct interaction; disruption of PICH-Plk1 interaction or PICH ATPase activity causes defects in chromosome compaction and anaphase bridge formation, placing PICH-Plk1 complex upstream of chromosome architecture regulation. Co-immunoprecipitation, siRNA depletion, overexpression of binding-deficient mutants, immunofluorescence Cell cycle Medium 18418076
2010 PICH and Plk1 coordinately maintain prometaphase chromosome arm architecture; PICH knockdown causes loss of Plk1 from chromosome arms and disorganized chromosomes; this disorganization is prevented by topoisomerase II inhibitor ICRF-193, implicating Topo II activity downstream. siRNA knockdown, immunofluorescence, ICRF-193 treatment Molecular biology of the cell Medium 20130082
2011 PICH binds directly to BLM and is required for BLM localization to anaphase centromeric threads; purified recombinant PICH has nucleosome remodeling activity in vitro; PICH and BLM cooperate to maintain anaphase DNA threads free of histones. Co-immunoprecipitation, siRNA depletion, in vitro nucleosome remodeling assay with purified protein, immunofluorescence The EMBO journal High 21743438
2012 PICH ATPase activity is required for prevention of chromatin bridge formation and for temporal/spatial control of PICH localization to chromatin, but is not required for UFB resolution; Plk1 controls PICH localization through phosphorylation of proteins distinct from PICH itself. Antibody microinjection, siRNA rescue with ATPase mutants, immunofluorescence, quantitative UFB analysis Chromosoma Medium 22527115
2012 BLM and PICH co-localize at centromeres from G2/prophase through anaphase; both proteins are required for recruitment of active topoisomerase IIα to centromeres; loss of either causes centromeric non-disjunction and increased UFBs, suggesting BLM-PICH cooperate upstream of Topo IIα in centromere decatenation. Immunofluorescence, siRNA, FISH, ChIP, electron microscopy, chromosome spreads PloS one Medium 22563370
2013 PICH binds duplex DNA with remarkably high affinity that increases with tension-induced DNA stretching; PICH translocates along DNA in an ATP-dependent manner and extension of DNA; binding of PICH diminishes force-induced DNA melting, supporting a model where PICH recognizes and stabilizes DNA under tension during anaphase. Microfluidics, fluorescence microscopy, optical tweezers, in vitro biochemical assays with purified PICH Molecular cell High 23973328
2015 PICH deletion in avian (DT40) cells causes chromosome structural abnormalities and hypersensitivity to Topo II inhibitor ICRF-193; PICH-deficient cells undergo sister chromatid non-disjunction; purified PICH strongly stimulates the catalytic activity of Topoisomerase II in vitro; PICH co-localizes with Topo IIα on UFBs and rDNA, and resolution of both requires PICH ATPase activity. Gene deletion (PICH-/- avian cells), in vitro Topo II stimulation assay with purified proteins, immunofluorescence, ICRF-193 sensitivity assays, human PICH-/- cell line generation Nature communications High 26643143
2015 PICH is SUMOylated by SUMO2/3 on mitotic chromosomes in a PIASy-dependent manner; PICH directly interacts with SUMOylated proteins (including SUMOylated PARP1 and Topo IIα); SUMOylation of PICH reduces its DNA binding capability, suggesting SUMO regulates PICH DNA-dependent ATPase activity. Xenopus egg extract assays, purified recombinant human PICH binding assays, in vitro SUMOylation, DNA binding assays The Journal of biological chemistry High 25564610
2016 PICH contains three SUMO-interacting motifs (SIMs); SIM3 (near the C-terminus) is critical for centromeric localization, while the other two SIMs function in chromatin bridge prevention; all SIMs are dispensable for PICH localization on UFBs. Conditional PICH expression, SIM-deficient mutant analysis, immunofluorescence, siRNA rescue Cell cycle Medium 27230136
2017 PICH interacts with BEND3 via a novel interface between a TPR domain in PICH and a BEN domain in BEND3; this interaction occurs in mitosis; the crystal structure of the TPR-BEN complex was determined at 2.2 Å resolution and key residues for the interaction were identified. Co-immunoprecipitation, in vitro pulldown with purified proteins, X-ray crystallography, site-directed mutagenesis Nucleic acids research High 28977671
2018 Loss of PICH in mice causes embryonic lethality at E12.5 due to global DNA damage accumulation, chromosomal instability, p53 activation, and increased apoptosis; p53 deletion does not rescue viability; PICH-deficient MEFs are resistant to RASV12/E1A transformation. Pich knockout mouse generation, embryo phenotyping, immunofluorescence, p53 double-KO epistasis Cell reports High 30232008
2019 PICH and Topoisomerase 3α (TOP3A) combine to introduce positive DNA supercoiling into DNA: PICH progressively extrudes hypernegatively supercoiled DNA loops that are relaxed by TOP3A, creating an extraordinarily high density of positive supercoiling analogous to reverse-gyrase activity. In vitro reconstitution with purified PICH and TOP3A, single-molecule magnetic tweezers, fluorescence imaging Nature structural & molecular biology High 30936532
2020 Upon replication stress, TOP2A is recruited to stalled forks, then SUMOylated by ZATT, which recruits the SUMO-targeted DNA translocase PICH; PICH promotes extensive fork reversal; disruption of the ZATT-TOP2A-PICH axis results in accumulation of partially reversed forks and genome instability. siRNA depletion, iPOND, proximity ligation assay, replication fiber assay, electron microscopy of replication intermediates Molecular cell High 33296677
2020 PICH specifically disperses SUMO2/3-modified proteins (including SUMOylated Topo IIα) from mitotic chromosomes in a translocase-dependent manner; PICH attenuates SUMOylated Topo IIα catalytic activity in vitro via its SUMO-binding ability. Auxin-inducible degron conditional depletion, immunofluorescence, in vitro SUMOylated Topo IIα activity assay with purified PICH Molecular biology of the cell Medium 32877270
2022 PICH is a tension- and ATP-dependent nucleosome remodeler: in a single-molecule assay mimicking chromatin under tension, PICH facilitates nucleosome unwrapping and slides remaining histones along DNA, providing direct evidence for its chromatin remodeling activity at anaphase bridges. Dual-trap optical tweezers, fluorescence imaging, single-molecule assay with purified PICH and nucleosome arrays Nature communications High 36433994
2022 PICH deficiency in mouse embryos causes defective embryonic hematopoiesis: PICH-KO fetal liver HSCs show elevated cytoplasmic dsDNA and activation of the cGAS-STING pathway leading to excessive type I interferon production; deletion of Ifnar1 or cGAS rescues the defective hematopoiesis. Pich-KO mouse model, bone marrow transplantation, cGAS/Ifnar1 epistasis, flow cytometry, cytoplasmic dsDNA staining Advanced science High 35037428
2022 PICH regulates the expression of Nrf2 and antioxidant response genes during oxidative stress; PICH is present on Nrf2 and antioxidant gene promoters (by ChIP); Nrf2 and H3K27ac occupancy at PICH target promoters depends on PICH expression. ChIP, siRNA depletion, overexpression rescue, RT-PCR, ROS measurement Epigenomes Low 36278682
2023 PICH forms a transcriptional complex with RNA polymerase II (Pol II) and ATF4 at the CCNA1 promoter in an ATPase-dependent manner, promoting cyclin A1 transcription and S-phase progression; this function contributes to 5-FU chemoresistance in gastric cancer. Co-immunoprecipitation of PICH-Pol II-ATF4 complex, ChIP, ATPase-deficient mutant rescue, human organoids, patient-derived xenografts Cancer research Medium 37646571
2023 ERCC6L (PICH) directly interacts with KIF4A; both proteins are involved in mitosis and the malignant progression of breast cancer; ERCC6L accelerates the cell cycle by regulating p53/p21/CDK1/Cyclin B and PLK1/CDC25C/CDK1/Cyclin B signaling pathways. Co-immunoprecipitation, ERCC6L conditional knockout mouse model, siRNA/overexpression functional assays, western blotting Journal of experimental & clinical cancer research Low 37667329
2023 A genome-wide loss-of-function screen identified FIRRM (C1orf112) as synthetic lethal with PICH (ERCC6L); FIRRM interacts with and stabilizes FIGNL1; loss of FIRRM or FIGNL1 causes UFB formation and impaired replication fork dynamics, creating dependence on PICH for viability. Genome-wide CRISPR KO screen, Co-IP, immunofluorescence, replication fork assays Cell reports Medium 37347663
2024 RAD52 deficiency increases ERCC6L-coated anaphase UFBs, and ERCC6L depletion causes elevated RAD52 foci in prometaphase and interphase cells; combined depletion of ERCC6L and CDK1 inhibition causes marked loss of viability in RAD52-deficient cells, indicating RAD52 and ERCC6L play compensatory roles in genome stability in mitosis. CRISPR KO screen, siRNA depletion, immunofluorescence, 53BP1 foci assay, hydroxyurea/ICRF-193 treatment PLoS genetics Medium 39561207
2025 PICH's translocase activity plays a dual role in UFB resolution: facilitating generation of single-stranded UFBs and stimulating topoisomerase IIα; a PICH mutant impairing BLM and RIF1 UFB recruitment partially inhibits resolution, while the translocase-inactive mutant (PICHK128A) fails to resolve UFBs and induces hypocondensed chromosomes; PICH depletion causes chromosomal rearrangements including translocations and inversions by whole-genome sequencing. siRNA depletion, PICH mutant rescue, whole-genome sequencing, immunofluorescence, DNA combing Nucleic acids research Medium 39704103
2025 PICH impacts the spindle assembly checkpoint (SAC): defects in either PICH remodeling activity or SIM-mediated SUMO binding delay mitotic progression via SAC activation (extended Mad1 foci at centromeres); PICH controls Bub1 kinetochore association, directly or indirectly affecting SAC activity. Conditional PICH depletion (AID system), PICH mutant replacement, proteomics of chromosomal SUMOylated proteins, immunofluorescence, live-cell imaging Life science alliance Medium 39919802

Source papers

Stage 0 corpus · 52 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 PICH, a centromere-associated SNF2 family ATPase, is regulated by Plk1 and required for the spindle checkpoint. Cell 287 17218258
2015 PICH promotes sister chromatid disjunction and co-operates with topoisomerase II in mitosis. Nature communications 98 26643143
2013 PICH: a DNA translocase specially adapted for processing anaphase bridge DNA. Molecular cell 88 23973328
2011 PICH and BLM limit histone association with anaphase centromeric DNA threads and promote their resolution. The EMBO journal 79 21743438
2007 Depletion of topoisomerase IIalpha leads to shortening of the metaphase interkinetochore distance and abnormal persistence of PICH-coated anaphase threads. Journal of cell science 67 17956945
2020 The ZATT-TOP2A-PICH Axis Drives Extensive Replication Fork Reversal to Promote Genome Stability. Molecular cell 65 33296677
2009 Re-examination of siRNA specificity questions role of PICH and Tao1 in the spindle checkpoint and identifies Mad2 as a sensitive target for small RNAs. Chromosoma 57 19904549
2001 Stabilization of local structures by pi-CH and aromatic-backbone amide interactions involving prolyl and aromatic residues. Protein engineering 51 11579222
2012 Bloom's syndrome and PICH helicases cooperate with topoisomerase IIα in centromere disjunction before anaphase. PloS one 50 22563370
2019 PICH and TOP3A cooperate to induce positive DNA supercoiling. Nature structural & molecular biology 37 30936532
2010 PICH and cotargeted Plk1 coordinately maintain prometaphase chromosome arm architecture. Molecular biology of the cell 37 20130082
2017 ERCC6L, a DNA helicase, is involved in cell proliferation and associated with survival and progress in breast and kidney cancers. Oncotarget 35 28178669
2012 On the regulation, function, and localization of the DNA-dependent ATPase PICH. Chromosoma 35 22527115
2008 Targeting Plk1 to chromosome arms and regulating chromosome compaction by the PICH ATPase. Cell cycle (Georgetown, Tex.) 31 18418076
2018 Loss of PICH Results in Chromosomal Instability, p53 Activation, and Embryonic Lethality. Cell reports 30 30232008
2016 PICH promotes mitotic chromosome segregation: Identification of a novel role in rDNA disjunction. Cell cycle (Georgetown, Tex.) 30 27565185
2019 Loss of PICH promotes chromosome instability and cell death in triple-negative breast cancer. Cell death & disease 29 31160555
2015 SUMOylation regulates polo-like kinase 1-interacting checkpoint helicase (PICH) during mitosis. The Journal of biological chemistry 25 25564610
2018 ERCC6L that is up-regulated in high grade of renal cell carcinoma enhances cell viability in vitro and promotes tumor growth in vivo potentially through modulating MAPK signalling pathway. Cancer gene therapy 24 30459398
2023 FIRRM/C1orf112 is synthetic lethal with PICH and mediates RAD51 dynamics. Cell reports 21 37347663
2019 ERCC6L promotes cell growth and invasion in human colorectal cancer. Oncology letters 21 31289493
2020 ERCC6L promotes the progression of hepatocellular carcinoma through activating PI3K/AKT and NF-κB signaling pathway. BMC cancer 20 32891122
2016 SUMO-interacting motifs (SIMs) in Polo-like kinase 1-interacting checkpoint helicase (PICH) ensure proper chromosome segregation during mitosis. Cell cycle (Georgetown, Tex.) 20 27230136
2018 shRNA knockdown of DNA helicase ERCC6L expression inhibits human breast cancer growth. Molecular medicine reports 17 30066865
2005 Ercc6l, a gene of SNF2 family, may play a role in the teratogenic action of alcohol. Toxicology letters 17 15917148
2022 PICH Supports Embryonic Hematopoiesis by Suppressing a cGAS-STING-Mediated Interferon Response. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 16 35037428
2023 PICH Activates Cyclin A1 Transcription to Drive S-Phase Progression and Chemoresistance in Gastric Cancer. Cancer research 14 37646571
2023 ERCC6L facilitates the onset of mammary neoplasia and promotes the high malignance of breast cancer by accelerating the cell cycle. Journal of experimental & clinical cancer research : CR 14 37667329
2022 PICH acts as a force-dependent nucleosome remodeler. Nature communications 14 36433994
2017 A novel TPR-BEN domain interaction mediates PICH-BEND3 association. Nucleic acids research 14 28977671
2020 PICH regulates the abundance and localization of SUMOylated proteins on mitotic chromosomes. Molecular biology of the cell 13 32877270
2020 Upregulation of Excision Repair Cross-Complementation Group 6-Like (ERCC6L) Promotes Tumor Growth in Hepatocellular Carcinoma. Digestive diseases and sciences 11 32347436
2022 A pan-cancer analysis of the oncogenic role of ERCC6L. BMC cancer 9 36550435
2021 ERCC6L promotes cell growth and metastasis in gastric cancer through activating NF-κB signaling. Aging 9 34425559
2022 ERCC6L is a biomarker and therapeutic target for non-small cell lung adenocarcinoma. Medical oncology (Northwood, London, England) 8 35150321
2021 Regulation of mitotic chromosome architecture and resolution of ultrafine anaphase bridges by PICH. Cell cycle (Georgetown, Tex.) 8 34530686
2023 ERCC6L facilitates the progression of laryngeal squamous cell carcinoma by the binding of FOXM1 and KIF4A. Cell death discovery 5 36726012
2023 Pan-genomic comparison of a potential solvent-tolerant alkaline protease-producing Exiguobacterium sp. TBG-PICH-001 isolated from a marine habitat. 3 Biotech 5 37854939
2016 Isolation and Proteomics Analysis of Barley Centromeric Chromatin Using PICh. Journal of proteome research 5 27142171
2016 Characterization of the NTPR and BD1 interacting domains of the human PICH-BEND3 complex. Acta crystallographica. Section F, Structural biology communications 5 27487930
2024 PICH deficiency limits the progression of MYC-induced B-cell lymphoma. Blood cancer journal 4 38253636
2007 Polo delivers a PICH to the kinetochore. Cell 4 17218250
2024 Anti-Proliferation Effect of Nodosin on Hepatocellular Carcinoma Cells Via The ERCC6L/PI3K/AKT/Axis. Journal of biochemical and molecular toxicology 2 39503234
2025 The interplay of the translocase activity and protein recruitment function of PICH in ultrafine anaphase bridge resolution and genomic stability. Nucleic acids research 1 39704103
2025 ERCC6L-mediated stabilization of HIF-1α enhances glycolysis and stemness properties of lung adenocarcinoma cells. Cell death & disease 1 40691138
2024 PICH, A protein that maintains genomic stability, can promote tumor growth. Gene 1 39491600
2024 RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis. PLoS genetics 1 39561207
2026 ERCC6L promotes cutaneous melanoma progression via PLK1-mediated aerobic glycolysis: Mechanisms and therapeutic implications. Life sciences 0 41564924
2026 PICH facilitates iPSC reprogramming by alleviating genomic instability induced by DNA replication stress. The FEBS journal 0 41981724
2025 PICH impacts the spindle assembly checkpoint via its DNA translocase and SUMO-interaction activities. Life science alliance 0 39919802
2023 RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis. bioRxiv : the preprint server for biology 0 37662271
2022 PLK-1 Interacting Checkpoint Helicase, PICH, Mediates Cellular Oxidative Stress Response. Epigenomes 0 36278682