Affinage

SMARCA5

SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 5 · UniProt O60264

Length
1052 aa
Mass
121.9 kDa
Annotated
2026-04-28
100 papers in source corpus 22 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMARCA5 (SNF2H) is the catalytic ATPase subunit of multiple mammalian ISWI chromatin-remodeling complexes—including NoRC, WICH, ACF/CHRAC, and RSF—that hydrolyze ATP to slide and regularly space nucleosomes, thereby controlling genome-wide nucleosome repeat length, linker DNA length, and chromatin accessibility (PMID:11532953, PMID:36630954, PMID:30996347). SMARCA5 is continuously required to maintain nucleosomal phasing and is essential for CTCF binding, enhancer insulation at TAD boundaries, and H2A.Z-associated chromatin organization; its acute depletion rapidly disrupts these features (PMID:30996347, PMID:36630954). Beyond steady-state chromatin maintenance, SMARCA5 is recruited to DNA replication foci via WSTF–PCNA interaction to preserve chromatin states during S phase, and to DNA double-strand breaks via PARP1/poly(ADP-ribose) where it facilitates RNF168-dependent ubiquitin signaling and heterochromatic DSB repair (PMID:15543136, PMID:23264744, PMID:25533843). SMARCA5 is essential for early embryonic development and hematopoietic differentiation, where it cooperates with nucleolin and lncRNAs such as lncMREF to open chromatin at lineage-specific gene promoters and enable p300/CBP-mediated H3K27 acetylation (PMID:14617767, PMID:28276606, PMID:32756943, PMID:36200826).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1998 Medium

    Identification of SMARCA5 as the human ISWI homolog established that SWI2/SNF2-family ATP-dependent chromatin remodeling is conserved in mammals.

    Evidence cDNA cloning, sequence homology, FISH mapping to 4q31

    PMID:9730600

    Open questions at the time
    • No biochemical activity demonstrated
    • No complex membership defined
  2. 2001 High

    Biochemical reconstitution revealed that SNF2H forms distinct ISWI complexes (ACF1-SNF2H and NoRC with TIP5), each capable of ATP-dependent nucleosome sliding, establishing SMARCA5 as a shared catalytic engine for multiple remodeling assemblies.

    Evidence Recombinant complex reconstitution, nucleosome sliding assays, co-IP, nucleolar colocalization

    PMID:11359880 PMID:11532953

    Open questions at the time
    • Functional distinction between complexes in vivo unclear
    • No genome-wide chromatin phenotype yet
  3. 2002 High

    Discovery of the WICH complex (WSTF–SNF2H) at replication foci and demonstration that ACF1-SNF2H is required for heterochromatin replication linked SMARCA5 to DNA replication-coupled chromatin assembly.

    Evidence Co-IP and biochemical purification from Xenopus extracts, RNAi in mammalian cells, BrdU incorporation, cell-cycle analysis

    PMID:11980720 PMID:12434153

    Open questions at the time
    • Mechanism by which remodeling facilitates replication fork progression unresolved
    • Relative contributions of WICH vs. ACF unclear
  4. 2003 High

    Genetic knockout established that Snf2h is essential for periimplantation development and hematopoietic erythropoiesis, demonstrating that ISWI remodeling is indispensable for mammalian cell viability and lineage differentiation.

    Evidence Gene targeting in mice (null mutation), blastocyst outgrowth, antisense knockdown in human CD34+ progenitors

    PMID:14617767

    Open questions at the time
    • Downstream chromatin targets in embryo not identified
    • Molecular basis of erythroid block unclear
  5. 2004 High

    The mechanism of SMARCA5 recruitment to replication foci was resolved: WSTF directly binds PCNA, tethering SNF2H to nascent chromatin; loss of either subunit causes aberrant heterochromatin compaction, revealing WICH as a chromatin maintenance factor during replication.

    Evidence Co-IP, GST pulldown (WSTF–PCNA), RNAi, chromatin fractionation

    PMID:15543136

    Open questions at the time
    • Whether WICH remodels specific loci vs. acts globally at forks not determined
  6. 2012 High

    SMARCA5 was placed in the DNA double-strand break repair pathway: PARP1-dependent recruitment of SNF2H to DSBs promotes RNF168 accumulation and ubiquitin signaling, enabling BRCA1 assembly and efficient repair.

    Evidence Live-cell imaging, co-IP, RNAi, clonogenic survival, comet assay

    PMID:23264744

    Open questions at the time
    • Direct biochemical mechanism of RNF168 activation by SNF2H not shown
    • Relative contribution vs. other remodelers at DSBs unclear
  7. 2014 High

    Multiple studies dissected SMARCA5's roles in specialized DNA damage contexts: at UV lesions, its ATPase and SLIDE domains enable CSB binding and transcription recovery; at heterochromatic DSBs, the ACF1-SNF2H complex acts downstream of KAP-1/CHD3.1 to relax compacted chromatin for Artemis-dependent repair; and NuMA controls SNF2H nucleoplasmic dynamics and accumulation at breaks.

    Evidence Laser micro-irradiation with domain mutants, siRNA epistasis with CHD3.1/RNF20/KAP-1, FRAP, DR-GFP reporter

    PMID:24753406 PMID:24990377 PMID:25533843

    Open questions at the time
    • Whether NuMA–SNF2H interaction is direct or bridged not resolved
    • Structural basis of SLIDE/ATPase domain requirement at UV lesions unknown
  8. 2017 High

    Conditional hematopoietic knockout revealed that Smarca5 is required for erythroid maturation in vivo; its loss activates p53-dependent DNA damage checkpoints and G2/M arrest in erythroblasts, linking chromatin remodeling to genome integrity during rapid proliferation.

    Evidence Conditional KO (Vav1-iCre, Epor-iCre), flow cytometry, western blot

    PMID:28276606

    Open questions at the time
    • Whether p53 activation reflects replication stress or transcriptional defects not distinguished
  9. 2019 High

    Genome-wide analyses in SNF2H-knockout ESCs established that SMARCA5 is the dominant nucleosome spacing factor: its loss increases nucleosome repeat length, selectively abolishes CTCF binding (but not REST), and disrupts TAD insulation, revealing transcription-factor-specific dependence on ISWI remodeling.

    Evidence Genetic KO in mESCs, MNase-seq, ATAC-seq, ChIP-seq, Hi-C

    PMID:30996347

    Open questions at the time
    • Mechanism by which spacing enables CTCF but not REST binding unresolved
    • Whether other ISWI ATPases compensate partially not addressed
  10. 2021 High

    SMARCA5 was shown to cooperate with nucleolin to open chromatin at hematopoietic gene promoters, enabling p300/CBP recruitment and H3K27ac deposition, providing a direct mechanism for how ISWI remodeling controls lineage-specific transcription.

    Evidence Co-IP, ATAC-seq, ChIP-seq, RNA-seq in zebrafish HSPCs

    PMID:32756943

    Open questions at the time
    • Whether nucleolin–SMARCA5 interaction is conserved in mammalian HSPCs not tested
    • Specificity of nucleolin vs. other SMARCA5 partners at these loci unclear
  11. 2022 High

    Two studies extended SMARCA5's partnership repertoire: it interacts with the NUP98-NSD1 oncofusion in phase-separated condensates and is essential for NUP98-NSD1-driven leukemic transformation; separately, the lncRNA lncMREF recruits SMARCA5 to myogenic gene promoters to open chromatin for p300/H3K27ac and drive muscle regeneration.

    Evidence AP-MS, PLA, inducible KD, pharmacological inhibition (NUP98-NSD1); RIP, ATAC-seq, ChIP-seq, in vivo muscle regeneration (lncMREF)

    PMID:35073946 PMID:36200826

    Open questions at the time
    • Whether lncMREF directly guides SMARCA5 to specific genomic loci or acts indirectly not established
    • Therapeutic window for SMARCA5 inhibition in NUP98-NSD1 leukemia unknown
  12. 2023 High

    Acute endogenous degradation of SMARCA5 proved that it is continuously required—not just during initial assembly—to maintain nucleosome repeat length and phasing throughout the cell cycle, with particular importance at G1/S and S phase for CTCF and H2A.Z site organization.

    Evidence Auxin-inducible degron at endogenous locus, MNase-seq, ChIP-seq, cell-cycle synchronization in three human cell lines

    PMID:36630954

    Open questions at the time
    • How SMARCA5 activity is regulated during the cell cycle not defined
    • Whether continuous requirement reflects active repositioning or counteracting disruptive forces unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: how SMARCA5 is differentially allocated among its multiple complexes in a cell-type-specific manner; the structural basis for its selectivity toward CTCF-flanking nucleosomes; and whether SMARCA5 can be therapeutically targeted in oncogenic contexts without compromising normal chromatin homeostasis.
  • No structure of full-length human SMARCA5 in complex with a partner subunit
  • Mechanism of cell-cycle-dependent regulation unknown
  • No therapeutic index established for SMARCA5 inhibition

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140657 ATP-dependent activity 7 GO:0140096 catalytic activity, acting on a protein 4
Localization
GO:0005634 nucleus 3 GO:0005694 chromosome 3 GO:0005654 nucleoplasm 2 GO:0005730 nucleolus 1
Pathway
R-HSA-4839726 Chromatin organization 6 R-HSA-69306 DNA Replication 4 R-HSA-73894 DNA Repair 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1640170 Cell Cycle 3 R-HSA-74160 Gene expression (Transcription) 3
Complex memberships
ACF/CHRAC (ACF1-SNF2H)NoRC (TIP5-SNF2H)RSF (RSF1-SNF2H)WICH (WSTF-SNF2H)

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 SMARCA5 encodes hSNF2H, a human homolog of Drosophila ISWI with a conserved ATPase domain characteristic of the SWI2/SNF2 family, mapped to chromosome 4q31.1–q31.2, suggesting a role in chromatin remodeling in humans. cDNA cloning, sequence homology analysis, FISH mapping, Northern blot Cytogenetics and cell genetics Medium 9730600
2001 Mammalian SNF2H (SMARCA5) forms an ACF1-SNF2H chromatin-remodeling complex (related to Drosophila ACF/CHRAC) that assembles regularly spaced nucleosomal arrays in an ATP-dependent manner, with Snf2h enriched in proliferating cells consistent with replication-associated chromatin assembly. cDNA cloning, differential expression analysis, biochemical fractionation Journal of neurochemistry Medium 11359880
2001 SNF2H (SMARCA5) is the catalytic ATPase subunit of the nucleolar remodeling complex NoRC (with TIP5), which interacts with TTF-I and induces ATP- and histone H4 tail-dependent nucleosome sliding at the rDNA locus. Co-immunoprecipitation, recombinant complex reconstitution, nucleosome sliding assay, colocalization with UBF in nucleolus The EMBO journal High 11532953
2002 SMARCA5/SNF2H forms the WICH complex with WSTF (Williams Syndrome Transcription Factor), and both localize to replicating pericentric heterochromatin; mouse WSTF interacts specifically with the SNF2H isoform of ISWI. Purification from Xenopus egg extract, co-immunoprecipitation in mouse cells, immunofluorescence colocalization at heterochromatin replication foci The EMBO journal High 11980720
2002 An ACF1-SNF2H (SMARCA5) complex is specifically required for DNA replication through pericentromeric heterochromatin; RNAi depletion of ACF1 impairs late-S-phase replication of heterochromatin, and SNF2H depletion slows replication progression throughout S phase. RNAi depletion, BrdU incorporation/immunofluorescence, cell-cycle analysis, expression of ACF1 mutant unable to interact with SNF2H Nature genetics High 12434153
2003 Snf2h (SMARCA5) is required for early mouse development; Snf2h-null embryos die at the periimplantation stage with growth arrest and death of both trophectoderm and inner cell mass; reduction of Snf2h in human CD34+ hematopoietic progenitors inhibits cytokine-induced erythropoiesis. Gene targeting (null mutation in mice), blastocyst outgrowth assay, antisense inhibition in human hematopoietic progenitors, in vitro differentiation assay Proceedings of the National Academy of Sciences of the United States of America High 14617767
2004 SMARCA5/SNF2H is recruited to DNA replication foci through direct interaction of its partner WSTF with PCNA; depletion of WSTF or SNF2H causes compaction of newly replicated chromatin and increases heterochromatin markers including HP1β. Co-immunoprecipitation, GST pulldown, immunofluorescence at replication foci, RNAi knockdown, chromatin fractionation Nature cell biology High 15543136
2004 SMARCA5/SNF2H (hSNF2H) physically interacts with DNMT3B, HDAC1, HDAC2, HP1 proteins, and Suv39h1 in heterochromatic regions; endogenous hSNF2H is associated with DNA methyltransferase activity. Co-immunoprecipitation, GST pulldown, immunofluorescence colocalization Biochemical and biophysical research communications Medium 15120635
2004 SNF2H (SMARCA5) and BRG1 (SWI/SNF ATPase) both stimulate V(D)J cleavage of nucleosomal substrates by RAG proteins in an ATP-dependent manner, with SNF2H acting through nucleosome remodeling to increase DNA accessibility. In vitro V(D)J cleavage assay on polynucleosomal arrays, recombinant SNF2H remodeling The Journal of biological chemistry Medium 15201272
2009 SNF2H (SMARCA5) is a major mammalian ISWI ATPase; loss of SNF2H decreases nucleosomal phasing and increases linker lengths in vivo, and is required for CTCF binding and chromosomal insulation of topologically associated domains. Genetic knockout of SNF2H in mouse embryonic stem cells, MNase-seq, ChIP-seq for transcription factor binding, Hi-C for chromosomal folding Nature High 30996347
2010 SMARCA5 is part of the RSF (remodeling and spacing factor) complex with RSF-1; knockdown of SMARCA5 in breast cancer cells decreases cell proliferation and invasion, arrests the cell cycle, downregulates cyclin A and MMP2, and upregulates p21. siRNA knockdown, colony formation assay, Matrigel invasion assay, flow cytometry, western blot Tumour biology Medium 25377162
2012 SMARCA5/SNF2H is recruited to DNA double-strand breaks in a PARP1-dependent manner; SMARCA5 interacts with RNF168 (which becomes poly(ADP-ribosyl)ated) in a DNA damage- and PARP-dependent manner, and promotes RNF168 accumulation at DSBs, thereby facilitating ubiquitin conjugation and BRCA1 assembly; SMARCA5 depletion renders cells sensitive to ionizing radiation and causes DSB repair defects. Live cell imaging, co-immunoprecipitation, RNAi depletion, immunofluorescence, clonogenic survival, comet assay Journal of cell science High 23264744
2014 SMARCA5/SNF2H and its binding partners ACF1 and WSTF are rapidly recruited to UV-C-induced DNA damage in a transcription- and histone-modification-dependent manner; recruitment requires the SWI2/SNF2-ATPase and SLIDE domains of SMARCA5; SMARCA5 facilitates CSB binding to lesion-stalled RNA Pol II and promotes transcription recovery; after initial recruitment, SMARCA5 relocalizes away from DNA damage center in a HAND-domain-dependent manner. Live cell imaging (laser micro-irradiation), domain deletion mutants, siRNA knockdown, transcription recovery assays Nucleic acids research High 24990377
2014 ACF1-SNF2H (SMARCA5) ISWI complex is required for Artemis-dependent DSB repair in heterochromatin; ACF1-SNF2H requires RNF20 for binding to heterochromatic DSBs and functions downstream of pKAP-1-mediated CHD3.1 dispersal to relax compacted chromatin; CHD3.1 and ACF1-SNF2H display counteractive chromatin remodeling activities. siRNA knockdown, live-cell imaging, comet assay, epistasis analysis, chromatin compaction assays The Journal of cell biology High 25533843
2014 NuMA interacts with SMARCA5/SNF2H via co-immunoprecipitation, regulates SNF2H diffusion in the nucleoplasm, and controls its accumulation at DNA double-strand breaks; cells with silenced NuMA show reduced chromatin decompaction after DNA cleavage and impaired homologous recombination repair. Co-immunoprecipitation, FRAP, siRNA knockdown, DR-GFP reporter assay, laser micro-irradiation Nucleic acids research Medium 24753406
2014 SMARCA5 (Smarca5) supports CTCF binding to target sites on chromatin, facilitates CTCF's enhancer-blocking function at the ICR, and is recruited with CTCF and the Cohesin complex to the SPI1 gene enhancer during myeloid differentiation, where it helps control PU.1 expression. Chromatin immunoprecipitation (ChIP), co-immunoprecipitation, siRNA knockdown, AZA-mediated demethylation experiments PloS one Medium 24498324
2017 Conditional deletion of Smarca5 at the onset of definitive hematopoiesis causes late fetal anemia; hematopoietic stem and progenitor cells accumulate but cannot mature; loss of Smarca5 leads to increased p53 levels phosphorylated at S15 (DNA damage) and acetylated at K376 (CBP/p300), activation of p53 targets, and G2/M block in basophilic erythroblasts. Conditional gene knockout (Vav1-iCre and Epor-iCre), flow cytometry, western blot, 4-OHT-mediated ex vivo deletion Stem cells (Dayton, Ohio) High 28276606
2019 Loss of SNF2H (SMARCA5) in mouse embryonic stem cells decreases nucleosomal phasing and increases linker lengths; SNF2H loss selectively impairs binding of CTCF but not REST, revealing that different transcription factors rely on distinct remodeling pathways, and that SNF2H is required for topological insulation at TAD boundaries. Genetic knockout, MNase-seq, ATAC-seq, ChIP-seq, Hi-C Nature High 30996347
2021 Smarca5 interacts with nucleolin to promote chromatin accessibility at promoters of hematopoiesis-related genes in fetal HSPCs, thereby facilitating genomic binding of p300/CBP/H3K27ac to upregulate expression of bcl11ab and other hematopoietic regulators. Co-immunoprecipitation, ATAC-seq, RNA-seq, ChIP-seq, zebrafish genetic model Blood High 32756943
2022 SMARCA5 interacts with the NUP98-NSD1 oncofusion protein within phase-separated nuclear condensates; SMARCA5 is an essential mediator of NUP98-NSD1-driven hematopoietic cell transformation, with its enzymatic activity (not condensate formation) required for maintenance of the transformed phenotype. Affinity purification–mass spectrometry, proximity ligation assay, inducible knockdown, pharmacological inhibition, methylcellulose colony assay Journal of experimental & clinical cancer research Medium 35073946
2022 The lncRNA lncMREF interacts with Smarca5 in differentiating muscle satellite cells to promote chromatin accessibility, thereby facilitating genomic binding of p300/CBP/H3K27ac and upregulating expression of myogenic regulators including MyoD, promoting myogenic differentiation and muscle regeneration. RNA immunoprecipitation, ATAC-seq, ChIP-seq, co-immunoprecipitation, loss-of-function/gain-of-function in vitro and in vivo Nucleic acids research High 36200826
2023 SMARCA5 is continuously required to maintain nucleosome repeat length and nucleosomal phasing in human cells; acute degradation of endogenous SMARCA5 (via auxin-inducible degron) rapidly increases global nucleosome repeat length; SMARCA5 co-localizes with CTCF and H2A.Z, and its loss causes rapid loss of CTCF DNA binding and disruption of nucleosomal phasing around CTCF sites; SMARCA5 is specifically required for nucleosome spacing control at G1/S and during S phase. Auxin-inducible degron system (endogenous tagging), MNase-seq, ChIP-seq, cell-cycle synchronization in three human cell lines Molecular cell High 36630954
2010 An in-frame fusion of EWSR1 (exons 1–7) to SMARCA5 (exons 14–32) was identified in an extraskeletal Ewing sarcoma/PNET with t(4;22)(q31;q12); NIH3T3 cells expressing EWSR1-hSNF2H exhibit anchorage-independent growth; deletion of the C-terminus (SLIDE/SANT motifs) impairs, and deletion of the SNF2_N domain fully abrogates, NIH3T3 cell transformation. FISH, RACE, RT-PCR, sequencing, soft-agar colony formation assay, domain deletion analysis Modern pathology Medium 21113140

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 ACF, an ISWI-containing and ATP-utilizing chromatin assembly and remodeling factor. Cell 527 9230310
1997 Chromatin-remodelling factor CHRAC contains the ATPases ISWI and topoisomerase II. Nature 436 9252192
1995 ISWI, a member of the SWI2/SNF2 ATPase family, encodes the 140 kDa subunit of the nucleosome remodeling factor. Cell 322 8521502
1999 Nucleosome movement by CHRAC and ISWI without disruption or trans-displacement of the histone octamer. Cell 296 10399913
1999 ACF consists of two subunits, Acf1 and ISWI, that function cooperatively in the ATP-dependent catalysis of chromatin assembly. Genes & development 276 10385622
2002 An ACF1-ISWI chromatin-remodeling complex is required for DNA replication through heterochromatin. Nature genetics 249 12434153
2001 NoRC--a novel member of mammalian ISWI-containing chromatin remodeling machines. The EMBO journal 242 11532953
2003 Crystal structure and functional analysis of a nucleosome recognition module of the remodeling factor ISWI. Molecular cell 218 14536084
2019 Mammalian ISWI and SWI/SNF selectively mediate binding of distinct transcription factors. Nature 204 30996347
2003 PIE1, an ISWI family gene, is required for FLC activation and floral repression in Arabidopsis. The Plant cell 200 12837955
1999 ISWI is an ATP-dependent nucleosome remodeling factor. Molecular cell 199 10078206
2002 WSTF-ISWI chromatin remodeling complex targets heterochromatic replication foci. The EMBO journal 194 11980720
2000 HuCHRAC, a human ISWI chromatin remodelling complex contains hACF1 and two novel histone-fold proteins. The EMBO journal 184 10880450
2002 Modulation of ISWI function by site-specific histone acetylation. EMBO reports 180 11882543
2002 Biological functions of the ISWI chromatin remodeling complex NURF. Genes & development 177 12502740
2000 Active remodeling of somatic nuclei in egg cytoplasm by the nucleosomal ATPase ISWI. Science (New York, N.Y.) 176 11009424
2001 Nucleosome mobilization and positioning by ISWI-containing chromatin-remodeling factors. Journal of cell science 162 11683384
2003 The ISWI ATPase Snf2h is required for early mouse development. Proceedings of the National Academy of Sciences of the United States of America 161 14617767
2006 Analysis of nucleosome repositioning by yeast ISWI and Chd1 chromatin remodeling complexes. The Journal of biological chemistry 158 16606615
2004 The Williams syndrome transcription factor interacts with PCNA to target chromatin remodelling by ISWI to replication foci. Nature cell biology 158 15543136
2000 dMi-2 and ISWI chromatin remodelling factors have distinct nucleosome binding and mobilization properties. The EMBO journal 154 10944116
2004 Multiple roles for ISWI in transcription, chromosome organization and DNA replication. Biochimica et biophysica acta 150 15020052
2017 ISWI chromatin remodellers sense nucleosome modifications to determine substrate preference. Nature 145 28767641
2013 ISWI remodelers slide nucleosomes with coordinated multi-base-pair entry steps and single-base-pair exit steps. Cell 130 23374341
2012 Regulation of ISWI involves inhibitory modules antagonized by nucleosomal epitopes. Nature 128 23143334
2003 Evidence for DNA translocation by the ISWI chromatin-remodeling enzyme. Molecular and cellular biology 123 12612068
2007 ISWI regulates higher-order chromatin structure and histone H1 assembly in vivo. PLoS biology 121 17760505
2001 Acf1, the largest subunit of CHRAC, regulates ISWI-induced nucleosome remodelling. The EMBO journal 121 11447119
2012 Poly(ADP-ribosyl)ation links the chromatin remodeler SMARCA5/SNF2H to RNF168-dependent DNA damage signaling. Journal of cell science 119 23264744
2002 ISWI remodeling complexes in Xenopus egg extracts: identification as major chromosomal components that are regulated by INCENP-aurora B. Molecular biology of the cell 117 11809820
2002 A critical epitope for substrate recognition by the nucleosome remodeling ATPase ISWI. Nucleic acids research 116 11809876
2001 ISWI induces nucleosome sliding on nicked DNA. Molecular cell 112 11741543
2001 In vivo chromatin remodeling by yeast ISWI homologs Isw1p and Isw2p. Genes & development 103 11238381
2014 ISWI chromatin remodeling complexes in the DNA damage response. Cell cycle (Georgetown, Tex.) 97 25486562
2019 Using circular RNA SMARCA5 as a potential novel biomarker for hepatocellular carcinoma. Clinica chimica acta; international journal of clinical chemistry 93 30716279
2004 DNMT3B interacts with hSNF2H chromatin remodeling enzyme, HDACs 1 and 2, and components of the histone methylation system. Biochemical and biophysical research communications 92 15120635
2004 ACF1 improves the effectiveness of nucleosome mobilization by ISWI through PHD-histone contacts. The EMBO journal 91 15457208
2004 ISWI complexes in Saccharomyces cerevisiae. Biochimica et biophysica acta 85 15020051
2001 Cloning and characterization of the murine Imitation Switch (ISWI) genes: differential expression patterns suggest distinct developmental roles for Snf2h and Snf2l. Journal of neurochemistry 85 11359880
2019 Structures of the ISWI-nucleosome complex reveal a conserved mechanism of chromatin remodeling. Nature structural & molecular biology 84 30872815
2014 ISWI proteins participate in the genome-wide nucleosome distribution in Arabidopsis. The Plant journal : for cell and molecular biology 84 24606212
2007 A novel ISWI is involved in VSG expression site downregulation in African trypanosomes. The EMBO journal 84 17431399
2010 Human ISWI chromatin-remodeling complexes sample nucleosomes via transient binding reactions and become immobilized at active sites. Proceedings of the National Academy of Sciences of the United States of America 82 20974961
2017 Expansion of the ISWI chromatin remodeler family with new active complexes. EMBO reports 81 28801535
2010 A novel t(4;22)(q31;q12) produces an EWSR1-SMARCA5 fusion in extraskeletal Ewing sarcoma/primitive neuroectodermal tumor. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 81 21113140
2011 Chromatin remodelling in mammalian cells by ISWI-type complexes--where, when and why? The FEBS journal 77 21810179
2016 Structure and regulation of the chromatin remodeller ISWI. Nature 74 27919072
2012 The ATPase domain of ISWI is an autonomous nucleosome remodeling machine. Nature structural & molecular biology 72 23202585
2013 ISWI and CHD chromatin remodelers bind promoters but act in gene bodies. PLoS genetics 70 23468649
2021 The emerging role of ISWI chromatin remodeling complexes in cancer. Journal of experimental & clinical cancer research : CR 68 34736517
2004 Functional diversity of ISWI complexes. Biochemistry and cell biology = Biochimie et biologie cellulaire 68 15284901
1998 Cloning and mapping of SMARCA5 encoding hSNF2H, a novel human homologue of Drosophila ISWI. Cytogenetics and cell genetics 68 9730600
1998 Chromatin remodeling mediated by Drosophila GAGA factor and ISWI activates fushi tarazu gene transcription in vitro. Molecular and cellular biology 65 9566866
2014 Opposing ISWI- and CHD-class chromatin remodeling activities orchestrate heterochromatic DNA repair. The Journal of cell biology 64 25533843
2014 Human ISWI complexes are targeted by SMARCA5 ATPase and SLIDE domains to help resolve lesion-stalled transcription. Nucleic acids research 62 24990377
2018 The nucleosomal acidic patch relieves auto-inhibition by the ISWI remodeler SNF2h. eLife 61 29664398
2000 Multiple ISWI ATPase complexes from xenopus laevis. Functional conservation of an ACF/CHRAC homolog. The Journal of biological chemistry 60 10942776
2018 Involvement of circular RNA SMARCA5/microRNA-620 axis in the regulation of cervical cancer cell proliferation, invasion and migration. European review for medical and pharmacological sciences 59 30575898
2006 C. elegans ISWI and NURF301 antagonize an Rb-like pathway in the determination of multiple cell fates. Development (Cambridge, England) 59 16774993
2009 Chromatin remodeling by imitation switch (ISWI) class ATP-dependent remodelers is stimulated by histone variant H2A.Z. The Journal of biological chemistry 57 19940112
2020 Pioneer-like factor GAF cooperates with PBAP (SWI/SNF) and NURF (ISWI) to regulate transcription. Genes & development 55 33303640
2017 The role of ISWI chromatin remodeling complexes in brain development and neurodevelopmental disorders. Molecular and cellular neurosciences 54 29249292
2014 NuMA promotes homologous recombination repair by regulating the accumulation of the ISWI ATPase SNF2h at DNA breaks. Nucleic acids research 52 24753406
2019 Circular RNA SMARCA5 inhibits the proliferation, migration, and invasion of non-small cell lung cancer by miR-19b-3p/HOXA9 axis. OncoTargets and therapy 51 31564891
2019 Circ-SMARCA5 suppresses progression of multiple myeloma by targeting miR-767-5p. BMC cancer 48 31601173
2011 Genome-wide characterization of chromatin binding and nucleosome spacing activity of the nucleosome remodelling ATPase ISWI. The EMBO journal 48 21448136
2000 Chromatin remodeling gene SMARCA5 is dysregulated in primitive hematopoietic cells of acute leukemia. Leukemia 48 10914549
2014 Overexpression of SMARCA5 correlates with cell proliferation and migration in breast cancer. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 47 25377162
2009 Functional interplay between chromatin remodeling complexes RSC, SWI/SNF and ISWI in regulation of yeast heat shock genes. Nucleic acids research 47 20015969
2009 ISWI is a RanGTP-dependent MAP required for chromosome segregation. The Journal of cell biology 44 20008562
2011 Probing the conformation of the ISWI ATPase domain with genetically encoded photoreactive crosslinkers and mass spectrometry. Molecular & cellular proteomics : MCP 43 22167269
2022 Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex. Nucleic acids research 42 36200826
2020 Dual Recognition of H3K4me3 and DNA by the ISWI Component ARID5 Regulates the Floral Transition in Arabidopsis. The Plant cell 42 32358072
2017 The ISWI ATPase Smarca5 (Snf2h) Is Required for Proliferation and Differentiation of Hematopoietic Stem and Progenitor Cells. Stem cells (Dayton, Ohio) 42 28276606
2011 Binding kinetics of human ISWI chromatin-remodelers to DNA repair sites elucidate their target location mechanism. Nucleus (Austin, Tex.) 40 21738833
2023 Human SMARCA5 is continuously required to maintain nucleosome spacing. Molecular cell 39 36630954
2020 Circular RNA SMARCA5 may serve as a tumor suppressor in non-small cell lung cancer. Journal of clinical laboratory analysis 38 31944395
2011 SMARCA5 methylation and expression in gastric cancer. Cancer investigation 38 21261476
2007 Site-specific acetylation of ISWI by GCN5. BMC molecular biology 38 17760996
2004 ATP-dependent remodeling by SWI/SNF and ISWI proteins stimulates V(D)J cleavage of 5 S arrays. The Journal of biological chemistry 38 15201272
2019 Asymmetry between the two acidic patches dictates the direction of nucleosome sliding by the ISWI chromatin remodeler. eLife 37 31094676
2011 The ISWI chromatin remodeler organizes the hsrω ncRNA-containing omega speckle nuclear compartments. PLoS genetics 36 21637796
2005 Chromatin remodeling by WSTF-ISWI at the replication site: opening a window of opportunity for epigenetic inheritance? Cell cycle (Georgetown, Tex.) 35 15753658
2019 Structure of the primed state of the ATPase domain of chromatin remodeling factor ISWI bound to the nucleosome. Nucleic acids research 34 31402386
2010 A proposal for kinetic proof reading by ISWI family chromatin remodeling motors. Current opinion in chemical biology 34 20833099
2009 The ISWI-containing NURF complex regulates the output of the canonical Wingless pathway. EMBO reports 34 19713963
2009 Drosophila ISWI regulates the association of histone H1 with interphase chromosomes in vivo. Genetics 32 19380479
2020 Circ-SMARCA5 suppresses colorectal cancer progression via downregulating miR-39-3p and upregulating ARID4B. Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver 31 32807692
2014 ISWI chromatin remodeling: one primary actor or a coordinated effort? Current opinion in structural biology 31 24561830
2008 The chromatin remodelers ISWI and ACF1 directly repress Wingless transcriptional targets. Developmental biology 31 18786525
2014 Epigenetic control of SPI1 gene by CTCF and ISWI ATPase SMARCA5. PloS one 30 24498324
2013 The role of micro RNAs let7c, 100 and 218 expression and their target RAS, C-MYC, BUB1, RB, SMARCA5, LAMB3 and Ki-67 in prostate cancer. Clinics (Sao Paulo, Brazil) 30 23778407
2022 SMARCA5 interacts with NUP98-NSD1 oncofusion protein and sustains hematopoietic cells transformation. Journal of experimental & clinical cancer research : CR 29 35073946
2011 The chromatin remodeler ISWI regulates the cellular response to hypoxia: role of FIH. Molecular biology of the cell 29 21900490
2021 Smarca5-mediated epigenetic programming facilitates fetal HSPC development in vertebrates. Blood 28 32756943
2020 Nm23-H1 inhibits lung cancer bone-specific metastasis by upregulating miR-660-5p targeted SMARCA5. Thoracic cancer 27 32022430
2021 Circ SMARCA5 Inhibited Tumor Metastasis by Interacting with SND1 and Downregulating the YWHAB Gene in Cervical Cancer. Cell transplantation 26 33588586
2014 Regulation of ISWI chromatin remodelling activity. Chromosoma 26 24414837
2008 Genetic identification of a network of factors that functionally interact with the nucleosome remodeling ATPase ISWI. PLoS genetics 26 18535655
2006 The ISWI and CHD1 chromatin remodelling activities influence ADH2 expression and chromatin organization. Molecular microbiology 25 16468993