Affinage

INO80C

INO80 complex subunit C · UniProt Q6PI98

Length
192 aa
Mass
20.6 kDa
Annotated
2026-04-28
47 papers in source corpus 24 papers cited in narrative 24 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

INO80C is a conserved, multi-subunit ATP-dependent chromatin remodeling complex that slides nucleosomes, evicts the histone variant H2A.Z, and organizes genome-wide nucleosome arrays to regulate transcription, DNA repair, replication origin integrity, and higher-order chromatin architecture. Structurally, the Ino80 Snf2 ATPase motor engages nucleosomal DNA at the entry point (superhelical location −6), unwrapping ~15 bp and pumping DNA while the Arp5–Ies6 module grips the opposing nucleosome face as a counter-grip, together forming a ratchet mechanism in which Ies2 activates ATPase catalysis, Ies6–Arp5 promote nucleosome binding, and the Arp5 insertion domain couples hydrolysis to productive sliding (PMID:29643509, PMID:29643506, PMID:24297934, PMID:26306040). INO80C functions in homologous recombination by removing H2A.Z to enable presynaptic filament formation, in nucleotide excision repair by restoring chromatin after lesion excision, and in base excision repair through a translocation-independent facilitation of AP-site cleavage by APE1 (PMID:28514650, PMID:21135142, PMID:37696438). The complex also suppresses transcription–replication conflicts via Mec1/PAF1C-coupled RNA Pol II removal, prevents pervasive transcription at replication origins, and contributes to three-dimensional genome organization including promoter-anchored chromatin loops in embryonic stem cells (PMID:26798134, PMID:32905765, PMID:41642679).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2009 High

    Establishing that the Ino80 complex is an ATP-dependent nucleosome remodeler whose Iec1/YY1 subunit targets it to promoters for histone eviction answered the question of whether the complex has direct chromatin-remodeling activity and how it activates transcription.

    Evidence In vitro nucleosome remodeling assay, ChIP, and genetic deletion in fission yeast

    PMID:19933844

    Open questions at the time
    • Catalytic mechanism of DNA translocation not resolved
    • Subunit contributions to remodeling not individually dissected
    • Generality to other eukaryotes not tested
  2. 2010 High

    Placing INO80-C in the nucleotide excision repair pathway—recruited by Rad4-Rad23 to restore chromatin after UV lesion removal—established that INO80C acts post-repair to re-establish nucleosome structure rather than during lesion processing itself.

    Evidence Genetic epistasis, co-IP of Ino80–Rad4-Rad23, and modified ChIP tracking nucleosome reassembly in yeast

    PMID:21135142

    Open questions at the time
    • Whether INO80C deposits specific histones during restoration unknown
    • Mechanism of Rad4-dependent recruitment not structurally defined
  3. 2011 High

    Defining the modular architecture of human INO80—three modules assembling on distinct Ino80 ATPase domains—established which subunits constitute the minimal remodeling-competent core and which are metazoan-specific elaborations.

    Evidence Biochemical fractionation and reconstitution of human INO80 subassemblies with nucleosome remodeling assays

    PMID:21303910

    Open questions at the time
    • Structural organization of modules on nucleosomes unresolved
    • Functions of metazoan-specific N-terminal module unknown
  4. 2012 High

    Demonstrating that Ies6 loss causes ploidy increase and H2A.Z misincorporation at pericentric chromatin revealed that the Arp5–Ies6 module is essential for proper chromosome segregation through regulation of histone variant dynamics.

    Evidence Genetic deletion, flow cytometry, chromosome segregation assays, and ChIP in budding yeast

    PMID:23207916

    Open questions at the time
    • Whether Ies6 directly participates in H2A.Z eviction or only in nucleosome binding not separated
    • Mechanism connecting H2A.Z misincorporation to segregation defects unclear
  5. 2013 High

    Dissecting individual subunit contributions showed that Ies2 activates ATPase catalysis while Arp5–Ies6 promote nucleosome binding, establishing that substrate recognition and motor activation are separately regulated within the complex.

    Evidence In vitro ATPase and nucleosome binding assays with defined purified human subunit combinations

    PMID:24297934

    Open questions at the time
    • How Ies2 activates ATPase mechanistically not known
    • Structural basis for Ies6-mediated nucleosome recognition unresolved
  6. 2015 High

    Showing that the Arp5 insertion domain is required for nucleosome sliding but not ATPase stimulation uncoupled ATP hydrolysis from productive DNA translocation, identifying the insertion domain as the element that converts motor activity into nucleosome movement.

    Evidence Domain mutagenesis with in vitro ATPase and nucleosome sliding assays in yeast

    PMID:25964121 PMID:26306040

    Open questions at the time
    • Atomic structure of Arp5 insertion domain on nucleosome not yet available at this point
    • How insertion domain contacts the nucleosome surface unknown
  7. 2015 High

    Demonstrating that INO80C directly blocks H3K79 methylation by Dot1 and restricts Pol II transcription to gene units established a silencing/boundary function, showing INO80C prevents euchromatin invasion into heterochromatin.

    Evidence In vitro methylation block assay, ChIP-seq, genetic deletion, and nascent RNA analysis in yeast

    PMID:25691465

    Open questions at the time
    • Whether the block is via nucleosome positioning or direct Dot1 occlusion not resolved
    • Generality to mammalian heterochromatin not tested
  8. 2016 High

    Identifying that Mec1/ATR triggers INO80C- and PAF1C-dependent removal of RNAPII from transcribed genes near replication origins under stress revealed a checkpoint-directed mechanism by which INO80C resolves transcription–replication conflicts to permit fork restart.

    Evidence Genetic epistasis, ChIP, proteomics, and replication fork restart assays in budding yeast

    PMID:26798134

    Open questions at the time
    • Whether INO80C directly removes RNAPII or acts through chromatin restructuring not distinguished
    • How Mec1 signals to INO80C not biochemically defined
  9. 2018 High

    Near-atomic cryo-EM structures of INO80 bound to nucleosomes from both a thermophilic fungus and humans resolved the ratchet mechanism: the Snf2 motor at the DNA entry point pumps DNA while Arp5–Ies6 counter-grips the opposing face, with the Arp5 grappler contacting the H2A–H2B acidic patch—explaining how the unique motor positioning of INO80 drives sliding.

    Evidence Cryo-EM at 3.7–4.3 Å resolution with biochemical remodeling assays on both fungal and human complexes

    PMID:29643506 PMID:29643509

    Open questions at the time
    • Structural intermediates during the sliding cycle not captured
    • Mechanism of H2A.Z specificity for eviction versus canonical H2A not structurally explained
  10. 2017 High

    Genetic epistasis showing that H2A.Z deletion rescues presynaptic filament formation in INO80-deficient cells established that INO80C promotes homologous recombination specifically by evicting H2A.Z to permit Rad51 filament assembly.

    Evidence Genetic epistasis with double mutants, high-resolution HR assay, and live imaging in yeast

    PMID:28514650

    Open questions at the time
    • How H2A.Z inhibits Rad51 filament formation mechanistically unknown
    • Whether INO80C also contributes to later HR steps independently of H2A.Z not fully resolved
  11. 2020 High

    Showing that INO80C co-localizes with ORC at replication origins in yeast and mouse ESCs and suppresses pervasive transcription through origins linked INO80C-mediated nucleosome organization to prevention of origin-proximal DSBs and genomic instability.

    Evidence ChIP-seq, nascent transcript sequencing, DSB mapping, and genetic epistasis across yeast and mESCs

    PMID:32905765

    Open questions at the time
    • Whether INO80C acts at origins through H2A.Z exchange or canonical sliding not distinguished
    • Mechanism of origin-sequence-dependent but ORC-independent recruitment unknown
  12. 2021 Medium

    Demonstrating that INO80C loss impairs global chromatin decompaction (not just local DSB mobility) and that this limits strand invasion kinetics repositioned INO80C as a regulator of genome-wide chromatin accessibility required for efficient homology-directed repair.

    Evidence Live imaging of chromatin dynamics, genetic epistasis, and strand invasion kinetics in yeast

    PMID:32970994 PMID:33529595

    Open questions at the time
    • Whether INO80C-dependent decompaction requires histone eviction, ubiquitination, or both not fully resolved
    • Contribution of ubiquitin ligase recruitment versus direct remodeling not separated
  13. 2023 High

    Revealing that DNA damage (abasic sites, UV lesions) abolishes INO80C translocation while preserving nucleosome binding, yet INO80C still facilitates APE1 cleavage, defined a translocation-independent role in base excision repair distinct from its canonical sliding activity.

    Evidence In vitro DNA translocation, ATPase, and AP-site cleavage assays with purified damaged nucleosomes

    PMID:37696438

    Open questions at the time
    • Structural basis for how damage inhibits ATPase not determined
    • Mechanism by which static binding facilitates APE1 access unknown
  14. 2024 Medium

    Connecting cytoplasmic actin dynamics to nuclear INO80C activation showed that elevated nuclear G-actin stimulates INO80C to increase DNA polymerase processivity, and that excess INO80C activity converts single-strand lesions into DSBs during altered BER.

    Evidence Phosphoproteomics, auxin-induced degradation, genetic epistasis, and chromosome fragmentation assays in yeast

    PMID:39548059

    Open questions at the time
    • Direct biochemical mechanism by which G-actin stimulates INO80C not reconstituted
    • Relevance to mammalian cells not tested
  15. 2025 Medium

    Showing that INO80C loss alters chromatin subcompartments and promoter-anchored looping at bivalent regions in mESCs extended INO80C function beyond nucleosome positioning to three-dimensional genome organization.

    Evidence Hi-C, promoter capture Micro-C, ATAC-seq, and ChIP-seq in INO80C-depleted mouse ESCs

    PMID:41642679

    Open questions at the time
    • Whether loop changes are direct consequences of local nucleosome remodeling or indirect effects not resolved
    • Role of specific subunits in 3D organization not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for H2A.Z-specific eviction versus canonical H2A sliding, the mechanism of the translocation-independent BER function, how INO80C is recruited to replication origins independently of ORC, and whether the Arp5–Ies6 INO80-independent oncogenic function reflects a moonlighting activity.
  • No structural intermediate capturing H2A.Z eviction
  • Translocation-independent facilitation of APE1 lacks a structural or mechanistic model
  • INO80-independent Arp5–Ies6 function in cancer not biochemically reconstituted

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140657 ATP-dependent activity 6 GO:0042393 histone binding 3 GO:0003677 DNA binding 2
Localization
GO:0005694 chromosome 5 GO:0005634 nucleus 4
Pathway
R-HSA-4839726 Chromatin organization 7 R-HSA-73894 DNA Repair 5 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-69306 DNA Replication 2
Partners
ACTL6AACTR5ACTR8IES2INO80RUVBL1RUVBL2YY1
Complex memberships
INO80 chromatin remodeling complex

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 Cryo-EM structure of the evolutionarily conserved INO80 core complex from Chaetomium thermophilum bound to a nucleosome (4.3 Å global, 3.7 Å for major parts) revealed: Rvb1/Rvb2 AAA+ ATPase heterohexamer acts as a stator/scaffold; the Swi2/Snf2 ATPase motor binds nucleosomal DNA at superhelical location -6 and unwraps ~15 bp to pump entry DNA; Arp5 and Ies6 bind superhelical locations -2 and -3 as a counter grip; the Arp5 insertion domain forms a grappler element contacting the nucleosome dyad and H2A-H2B acidic patch. Together these elements form a macromolecular ratchet for nucleosome sliding and histone editing. Cryo-EM structure + biochemical remodeling assays Nature High 29643509
2018 Cryo-EM structure of human INO80 bound to nucleosome showed that INO80 motor domains are located on DNA at the nucleosome entry point (not at SHL2 as in other remodelers), and the ARP5-IES6 module makes contacts on the opposite side of the nucleosome. Uniquely, histone H3 tails regulate the INO80 motor domain activity. Cryo-EM structure of human INO80-nucleosome complex Nature High 29643506
2011 Human INO80 complex is organized into three modules assembling on distinct hIno80 ATPase domains: (i) N-terminal + metazoan-specific subunits (dispensable for remodeling); (ii) HSA/PTH domain with Arp4, Arp8, and YY1; (iii) Snf2 ATPase domain with Ies2, Ies6, Tip49a/b (RuvBL1/2), and Arp5. The core complex comprising HSA/PTH + Snf2 ATPase domains with YY1 and all conserved subunits is sufficient for ATP-dependent nucleosome remodeling. Biochemical fractionation, purification of subassemblies, ATP-dependent nucleosome remodeling assay Journal of Biological Chemistry High 21303910
2013 In human INO80, Ies2 (Ino Eighty Subunit 2) functions as a potent activator of the intrinsic ATPase activity of Ino80, while Ies6 and Arp5 function together to promote binding of the Ino80 ATPase to nucleosomes—demonstrating that substrate recognition and catalytic activity are separately regulated by distinct subunits. In vitro ATPase and nucleosome binding assays with purified subunit combinations PNAS High 24297934
2015 EM and 2D class averaging of yeast INO80-C and SWR-C revealed similar overall architectures with a dynamic 'tail' and compact 'head' containing Rvb1/Rvb2 as single heterohexameric rings. The Arp8/Arp4/Act1 module enhances nucleosome-binding affinity but is largely dispensable for remodeling, whereas the Ies6/Arp5 module is essential for INO80-C remodeling activity and controls conformational changes coupling nucleosome binding to remodeling. Electron microscopy, 2D class averaging, mass spectrometry, nucleosome remodeling assays with module deletions Nature Communications High 25964121
2016 Arp5 and Ies6 form a distinct, abundant subcomplex in vivo that stimulates INO80-mediated nucleosome remodeling activity in vitro. Their genomic occupancy correlates with nucleosome positioning at transcription start sites and expression of >1,000 INO80-regulated genes enriched in energy metabolism pathways; loss of arp5, ies6, or ino80 deregulates glycolysis/oxidative phosphorylation balance, raising mitochondrial potential. In vitro remodeling assays, ChIP-seq, genetic deletion phenotyping, metabolic measurements Molecular and Cellular Biology High 26755556
2016 Purified recombinant human minimal core INO80 complex (Ino80-truncated + actin, Arp4, Arp5, Arp8, Ies2, Ies6, Tip49a/b) has nucleosome sliding activity. Inositol hexaphosphate (IP6) is a non-competitive inhibitor that blocks the stimulatory effect of nucleosomes on ATPase activity by binding the C-terminal region of the Ino80 subunit. Ies2 and Arp5/Ies6 regulate ATPase activity synergistically to couple ATP hydrolysis to nucleosome sliding; an Arp5 bypass mutation restores ATPase in the absence of Ies2. Recombinant complex reconstitution in insect cells, nucleosome sliding and ATPase assays, inhibitor studies, bypass mutagenesis Nucleic Acids Research High 27257055
2015 Ies2 subunit is required for Arp5-Ies6 association with the catalytic components of the INO80 complex. Assembly of the Arp5-Ies6 module depends on conserved domains within Arp5, Ies6, and the spacer region of the Ino80 ATPase domain. Arp5-Ies6 interacts with chromatin only through assembly with the full INO80 complex. Ectopic Arp5-Ies6 stimulates ATPase and nucleosome sliding, but Arp5 lacking its unique insertion domain stimulates ATPase without promoting nucleosome sliding. Affinity purification, in vitro ATPase and nucleosome sliding assays, domain mutagenesis, ChIP Journal of Biological Chemistry High 26306040
2012 The Ies6 subunit is critical for INO80 function in vivo; loss of Ies6 or the Ino80 catalytic subunit leads to rapid ploidy increase, defective chromosome segregation, and altered pericentric chromatin structure due to misincorporation of H2A.Z into pericentric nucleosomes. Genetic deletion, flow cytometry (ploidy), chromosome segregation assays, chromatin immunoprecipitation Genes & Development High 23207916
2017 INO80-C performs at least two distinct functions during homologous recombination in yeast: DNA end resection and presynaptic filament formation. The second function is linked to H2A.Z removal; deletion of H2A.Z rescues presynaptic filament formation and HR in INO80-C-deficient cells, placing INO80-C-mediated H2A.Z eviction upstream of presynaptic filament assembly. Genetic epistasis (double mutants), high-resolution HR assay, live imaging of recombination intermediates Cell Reports High 28514650
2016 In budding yeast, Mec1 (ATR ortholog) triggers INO80C- and PAF1C-dependent removal of PAF1C and RNAPII from transcribed genes near early-firing origins under replication stress. Loss of INO80C (like paf1Δ or mec1 mutants) impairs replication fork restart after stalling, revealing genetic cooperation among Mec1, INO80C, and PAF1C in preventing transcription-replication conflicts. Genetic epistasis, ChIP, proteomics, replication fork restart assays Genes & Development High 26798134
2010 In yeast, INO80-C acts in the same genetic pathway as nucleotide excision repair (NER); Ino80 interacts with the NER damage recognition complex Rad4-Rad23 and is recruited to chromatin by Rad4 in a UV-damage-dependent manner. INO80-C is required for restoration of nucleosome structure after UV lesion repair (chromatin disruption during repair is normal but restoration is defective in ino80 mutants). Genetic epistasis, co-immunoprecipitation (Ino80-Rad4-Rad23), modified ChIP, UV sensitivity assays Journal of Cell Biology High 21135142
2015 Ino80 chromatin remodeling complex (Ino80C) directly prevents euchromatin invasion into transcriptionally silent chromatin and blocks H3K79 methylation by Dot1 in vitro. Heterochromatin stimulates Ino80C binding in vitro and in vivo, positioning Ino80C as a silencing complex that restricts Pol II transcription to gene units. In vitro H3K79 methylation block assay, ChIP-seq, genetic deletion, nascent RNA analysis Genes & Development High 25691465
2020 INO80-C co-localizes with the origin recognition complex (ORC) at yeast replication origins and at replication initiation sites in mouse ESCs. In yeast, INO80-C recruitment to origins requires origin sequences but not ORC. INO80-C and Mot1/NC2 function to prevent pervasive transcription through origin sequences; absence of these factors leads to new DNA double-strand breaks, linking INO80C-mediated nucleosome remodeling at origins to genomic stability. ChIP-seq, genetic epistasis, nascent transcript sequencing, DSB mapping Cell Reports High 32905765
2021 Checkpoint- and INO80C-dependent recruitment of ubiquitin-conjugating factors (Rad6, Bre1, Pep5, Ufd4, Rsp5) to chromatin contributes to core and linker histone depletion after DNA damage, reducing chromatin compaction and enhancing DNA locus mobility. Loss of these factors compromises DNA strand invasion kinetics during homology-driven repair. Chromatin proteomics (damage-induced chromatome dynamics), genetic deletions, DNA repair kinetics assay Molecular Cell Medium 33529595
2009 In fission yeast, the Ino80 complex mediates ATP-dependent nucleosome remodeling in vitro. Deletion of ies6 (or arp8, ies2) causes defects in DNA damage repair, replication stress response, and nucleotide metabolism. The Iec1 subunit (YY1-related) is required for Ino80 binding to target gene promoters and subsequent histone loss on phosphate starvation, revealing that Iec1-Ino80C promotes transcription through nucleosome eviction. In vitro nucleosome remodeling assay, genetic deletion, ChIP, gene expression analysis Molecular and Cellular Biology High 19933844
2018 The INO80 complex sustains metabolic homeostasis by promoting TORC1-mediated signaling to chromatin: ino80 mutants exhibit defective transcriptional profiles and altered histone acetylation at TORC1-responsive genes. The Ies6 subunit module has a strikingly divergent genetic signature linking INO80 to metabolic homeostasis, including mitochondrial maintenance. Genetic screens, transcriptomics, histone acetylation ChIP, genetic interaction analysis PLoS Genetics Medium 29462149
2023 Abasic sites and UV-irradiation damage abolish the DNA translocation activity of INO80-C by compromising ATP hydrolysis in the Ino80 catalytic subunit, while nucleosome binding remains intact. INO80-C facilitates AP site cleavage by AP-endonuclease 1 (APE1) independently of its DNA translocation activity, defining a novel translocation-independent role in base excision repair. In vitro DNA translocation and ATPase assays with damaged nucleosomes, AP site cleavage assay with purified APE1 Journal of Biological Chemistry High 37696438
2024 Loss of cytoplasmic actin filaments (via TORC2 inhibition or Las17 degradation) raises nuclear G-actin levels, which stimulates INO80C activity to increase DNA polymerase processivity. Genetic ablation of INO80C activity provides partial resistance to yeast chromosome shattering (YCS), placing elevated INO80C activity as a contributor to conversion of single-strand lesions into double-strand breaks during altered base excision repair. Phosphoproteomics, auxin-induced protein degradation, genetic epistasis, chromosome fragmentation assays Nature Communications Medium 39548059
2018 Genomic analysis of human INO80-C identified two classes of targets: Canonical INO80 sites enriched for open chromatin and H3K27ac where all three INO80-C modules (RUVBL1/2, MCRS1, YY1) co-occupy; and Non-Canonical INO80 (NC-INO80) sites characterized by inaccessible chromatin and H3K27me3 where only the INO80 ATPase is present. Biochemical pulldown showed INO80-C and the H3K27 acetyltransferase P300 physically interact at canonical sites, while no interaction was detected with EZH2. ChIP-seq, ATAC-seq, co-immunoprecipitation G3 Medium 29432129
2022 ACTR5 (Arp5) and its interacting partner IES6 show HCC-specific functions distinct from other INO80 complex members, suggesting an INO80-independent mechanism of ACTR5/IES6 in supporting hepatocellular carcinoma proliferation through repression of CDKN2A and CDK/E2F-driven cell cycle signaling. CRISPR interference screen, CRISPR gene tiling, genetic epistasis, tumor growth assays Science Advances Medium 36563143
2021 Loss of INO80-C reduces histone occupancy and chromatin movement at double-strand breaks, impairing ectopic homology-directed repair (HDR), while nucleosome depletion (via Nhp6 loss) increases chromatin movement and HDR. Global histone depletion rather than DSB mobility per se is rate limiting for HDR, placing INO80-C as a regulator of global chromatin decompaction required for efficient strand invasion. Live imaging of chromatin dynamics, genetic epistasis, strand invasion kinetics assays Molecular Cell Medium 32970994
2026 Deletion of IES6 in S. cerevisiae reduces genome-wide nucleosome spacing by 3 bp and disrupts regular nucleosome arrays across most genes. IES6 deletion is synthetically lethal with deletion of the ISWI-family remodeler ISW2, indicating functional redundancy in nucleosome organization. INO80 binding directly predicts sites where Ies6 is required for nucleosome organization. MNase-seq (genome-wide nucleosome mapping), genetic synthetic lethality, ChIP-seq Scientific Reports Medium 41720950
2025 In mouse embryonic stem cells, loss of INO80C alters subcompartment organization and a subset of promoter-anchored chromatin looping interactions (detected by promoter capture Micro-C), particularly at bivalent chromatin regions bound by OCT4, SOX2, NANOG, and INO80 itself, revealing a role for INO80C in higher-order 3D genome organization beyond nucleosome positioning. Hi-C, promoter capture Micro-C, ATAC-seq, ChIP-seq in mESCs with INO80C loss Genetics Medium 41642679

Source papers

Stage 0 corpus · 47 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2018 Structural basis for ATP-dependent chromatin remodelling by the INO80 complex. Nature 194 29643509
2018 Structure and regulation of the human INO80-nucleosome complex. Nature 150 29643506
2003 From gene networks to gene function. Genome research 131 14656964
2004 Mutator genes for suppression of gross chromosomal rearrangements identified by a genome-wide screening in Saccharomyces cerevisiae. Proceedings of the National Academy of Sciences of the United States of America 126 15184655
2016 Mec1, INO80, and the PAF1 complex cooperate to limit transcription replication conflicts through RNAPII removal during replication stress. Genes & development 98 26798134
2011 Subunit organization of the human INO80 chromatin remodeling complex: an evolutionarily conserved core complex catalyzes ATP-dependent nucleosome remodeling. The Journal of biological chemistry 96 21303910
2021 PHYTOCHROME-INTERACTING FACTORs trigger environmentally responsive chromatin dynamics in plants. Nature genetics 94 34140685
2017 Genome-Wide CRISPR Screen for Essential Cell Growth Mediators in Mutant KRAS Colorectal Cancers. Cancer research 92 28954733
2021 The INO80 chromatin remodeling complex promotes thermomorphogenesis by connecting H2A.Z eviction and active transcription in Arabidopsis. Molecular plant 91 34242850
2016 Scan-associated distress in lung cancer: Quantifying the impact of "scanxiety". Lung cancer (Amsterdam, Netherlands) 81 27597289
2015 Structural analyses of the chromatin remodelling enzymes INO80-C and SWR-C. Nature communications 63 25964121
2017 The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination. Cell reports 62 28514650
2012 The INO80 chromatin remodeling complex prevents polyploidy and maintains normal chromatin structure at centromeres. Genes & development 56 23207916
2020 DNA Damage-Induced Nucleosome Depletion Enhances Homology Search Independently of Local Break Movement. Molecular cell 48 32970994
2014 INO80-C and SWR-C: guardians of the genome. Journal of molecular biology 47 25451604
2021 Damage-induced chromatome dynamics link Ubiquitin ligase and proteasome recruitment to histone loss and efficient DNA repair. Molecular cell 44 33529595
2016 The INO80 Complex Requires the Arp5-Ies6 Subcomplex for Chromatin Remodeling and Metabolic Regulation. Molecular and cellular biology 44 26755556
2010 The Ino80 chromatin-remodeling complex restores chromatin structure during UV DNA damage repair. The Journal of cell biology 43 21135142
2013 Multiple modes of regulation of the human Ino80 SNF2 ATPase by subunits of the INO80 chromatin-remodeling complex. Proceedings of the National Academy of Sciences of the United States of America 42 24297934
2019 Epigenetic silencing of a multifunctional plant stress regulator. eLife 40 31418686
2009 Fission yeast Iec1-ino80-mediated nucleosome eviction regulates nucleotide and phosphate metabolism. Molecular and cellular biology 40 19933844
2015 The Ino80 complex prevents invasion of euchromatin into silent chromatin. Genes & development 36 25691465
2016 Synergy and antagonism in regulation of recombinant human INO80 chromatin remodeling complex. Nucleic acids research 33 27257055
2019 Roles of the INO80 and SWR1 Chromatin Remodeling Complexes in Plants. International journal of molecular sciences 32 31533258
2018 The INO80 chromatin remodeler sustains metabolic stability by promoting TOR signaling and regulating histone acetylation. PLoS genetics 30 29462149
2015 Assembly of the Arp5 (Actin-related Protein) Subunit Involved in Distinct INO80 Chromatin Remodeling Activities. The Journal of biological chemistry 29 26306040
2015 A Pooling Genome-Wide Association Study Combining a Pathway Analysis for Typical Sporadic Parkinson's Disease in the Han Population of Chinese Mainland. Molecular neurobiology 26 26227905
2018 Identification of Two Distinct Classes of the Human INO80 Complex Genome-Wide. G3 (Bethesda, Md.) 21 29432129
2020 Genome-Wide Meta-Analyses of FTND and TTFC Phenotypes. Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco 15 31294817
2020 INO80C Remodeler Maintains Genomic Stability by Preventing Promiscuous Transcription at Replication Origins. Cell reports 15 32905765
2022 ACTR5 controls CDKN2A and tumor progression in an INO80-independent manner. Science advances 14 36563143
2020 NC2 complex is a key factor for the activation of catalase-3 transcription by regulating H2A.Z deposition. Nucleic acids research 14 32633757
2022 Integrated Chromatin Accessibility and Transcriptome Landscapes of 5-Fluorouracil-Resistant Colon Cancer Cells. Frontiers in cell and developmental biology 13 35252200
2016 Response to Comment on "A histone acetylation switch regulates H2A.Z deposition by the SWR-C remodeling enzyme". Science (New York, N.Y.) 10 27463666
2022 Distinct functions of three chromatin remodelers in activator binding and preinitiation complex assembly. PLoS genetics 8 35793348
2023 Dynamic coalescence of yeast Heat Shock Protein genes bypasses the requirement for actin. Genetics 6 36659814
2023 DNA-translocation-independent role of INO80 remodeler in DNA damage repairs. The Journal of biological chemistry 6 37696438
2021 RNAi and Ino80 complex control rate limiting translocation step that moves rDNA to eroding telomeres. Nucleic acids research 5 34244792
2024 Loss of cytoplasmic actin filaments raises nuclear actin levels to drive INO80C-dependent chromosome fragmentation. Nature communications 4 39548059
2024 TORC2 inhibition triggers yeast chromosome fragmentation through misregulated Base Excision Repair of clustered oxidation events. Nature communications 3 39548071
2021 Distinct roles of nucleosome sliding and histone modifications in controlling the fidelity of transcription initiation. RNA biology 3 33280509
2025 Bromodomain proteins IBD1 and IBD2 link histone acetylation to SWR1- and INO80-mediated H2A.Z regulation in Tetrahymena. Epigenetics & chromatin 2 40764940
2022 Identification of novel PIEZO1::CBFA2T3 and INO80C::SETBP1 fusion genes in an acute myeloid leukemia patient by RNA-seq. Molecular biology reports 2 36472727
2026 esBAF and INO80C fine-tune subcompartments and differentially regulate enhancer-promoter interactions. Genetics 0 41642679
2026 The Ies6 subunit is essential for INO80-mediated nucleosome organization. Scientific reports 0 41720950
2025 esBAF and INO80C fine-tune subcompartments and differentially regulate enhancer-promoter interactions. bioRxiv : the preprint server for biology 0 41000727
2025 Transcription elongation regulated by H2B deubiquitination and H2A.Z eviction enables fungal virulence. The New phytologist 0 41272392