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
2026-06-10
68 papers in source corpus 29 papers cited in narrative 29 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMARCA5 (hSNF2H/hISWI) is the human homologue of Drosophila ISWI and the catalytic ATPase subunit of ISWI-family chromatin remodeling machinery that uses its conserved SWI2/SNF2 ATPase domain to reposition and space nucleosomes, thereby setting chromatin accessibility across the genome (PMID:9730600, PMID:36630954). Acute degradation of SMARCA5 rapidly increases global nucleosome repeat length and compacts chromatin while leaving nascent transcription largely intact within hours, establishing nucleosome spacing as its primary, continuous activity throughout G1/S and S phase (PMID:36630954). A central output of this activity is CTCF-directed chromatin architecture: SMARCA5 co-localizes with CTCF and H2A.Z and is required for CTCF DNA binding and proper nucleosomal phasing around CTCF sites, and it associates with the Cohesin complex to support CTCF enhancer-blocking function (PMID:36630954, PMID:24498324). SMARCA5 also operates in genome maintenance, being recruited to DNA double-strand breaks in a PARP1/poly(ADP-ribosyl)ation-dependent manner—through ADP-ribosylation-driven chromatin relaxation rather than direct PAR binding—where it promotes RNF168 accumulation and ubiquitin signaling for repair (PMID:23264744, PMID:38170578), and to UV-damaged chromatin via its functional ATPase, SLIDE, and HAND domains to facilitate CSB recruitment and transcription recovery during nucleotide excision repair (PMID:24990377). It functions within ISWI cofactor complexes (ACF1/BAZ1A, BAZ2A/TIP5, RSF-1) and partners with sequence-specific and chromatin factors including DNMT3B, nucleolin, CTCF, and DMRT1 to fulfill context-specific roles in remodeling-dependent gene regulation (PMID:15120635, PMID:40743397, PMID:26666816, PMID:32756943, PMID:41282062, PMID:40837621). Through these activities SMARCA5 is essential for definitive hematopoiesis and erythroid/myeloid maturation, T and B lymphocyte development and germinal center formation, male meiosis and spermatogenesis, and cell-cycle progression, with its loss frequently triggering p53 activation, senescence, and chromatid-segregation defects (PMID:28276606, PMID:31068388, PMID:39297882, PMID:40743397, PMID:32197313, PMID:35269430). Its protein stability is maintained by USP3-mediated removal of K63-linked polyubiquitination (PMID:39500888).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 1998 Medium

    Established the molecular identity of SMARCA5 by cloning it as a human ISWI homologue, predicting a chromatin-remodeling ATPase before any function was tested.

    Evidence cDNA cloning, sequence homology, Northern blot and FISH mapping

    PMID:9730600

    Open questions at the time
    • No functional reconstitution of remodeling activity
    • No in vivo phenotype defined
  2. 2004 Medium

    Connected SMARCA5 to repressive epigenetic machinery, indicating it acts at heterochromatin in concert with DNA methylation and silencing factors.

    Evidence Co-IP, GST pull-down, immunofluorescence co-localization and ATPase assay in human cells

    PMID:15120635

    Open questions at the time
    • Interactions from a single lab without reciprocal genome-wide validation
    • Functional consequence of DNMT3B association not tested
  3. 2009 Medium

    Defined SMARCA5 as a global regulator of chromatin structure in vivo, predominantly euchromatic with effects on histone modification and heterochromatin organization.

    Evidence Confocal immunostaining and heterozygous mouse model

    PMID:19482671

    Open questions at the time
    • Heterozygous model gives partial loss-of-function only
    • Direct nucleosome-level mechanism not assayed
  4. 2012 High

    Placed SMARCA5 in the DNA double-strand break response, showing PARP1/PAR-dependent recruitment that drives RNF168 ubiquitin signaling and BRCA1 assembly.

    Evidence Reciprocal Co-IP, laser-damage live imaging, siRNA, IR sensitivity and PAR functional assays

    PMID:23264744

    Open questions at the time
    • Whether remodeling ATPase activity is required for RNF168 promotion not dissected here
    • Mechanism of PAR-dependent recruitment left to later work
  5. 2014 High

    Extended SMARCA5's DNA-damage role to nucleotide excision repair, showing domain-dependent recruitment to UV lesions and a requirement for transcription recovery.

    Evidence Live imaging, domain-deletion mutagenesis, UV-C damage and transcription recovery assays

    PMID:24990377

    Open questions at the time
    • Substrate nucleosome substrate at lesions not directly characterized
    • Relative contributions of ACF1/WSTF complexes not separated
  6. 2014 Medium

    Linked SMARCA5 to genome architecture by showing it facilitates CTCF binding and enhancer-blocking together with Cohesin, with a lineage-specific output at SPI1.

    Evidence ChIP, Co-IP and enhancer-blocking reporter assays in myeloid/AML cells

    PMID:24498324

    Open questions at the time
    • Direct vs indirect facilitation of CTCF binding unresolved at this stage
    • Genome-wide scope not yet established
  7. 2017 High

    Demonstrated that SMARCA5 is essential for definitive hematopoiesis, with loss blocking erythroid/myeloid maturation and activating p53.

    Evidence Multiple conditional-Cre knockout mouse models, hematopoietic phenotyping, p53 modification Western blots

    PMID:28276606

    Open questions at the time
    • Whether p53 activation is cause or consequence of the maturation block not fully resolved
    • Direct chromatin targets in HSPCs not mapped
  8. 2019 High

    Showed SMARCA5 is required for lymphocyte development, with stage-specific blocks and only partial p53-dependence, distinguishing remodeling defects from p53-driven death.

    Evidence Conditional knockout, flow cytometry, expression profiling, p53 epistasis

    PMID:31068388

    Open questions at the time
    • p53-independent component of the developmental block mechanistically undefined
    • Direct target loci at DN3/pro-B stages not identified
  9. 2020 Medium

    Implicated SMARCA5 in mitotic fidelity and chromatid cohesion, beyond its interphase chromatin roles.

    Evidence CRISPR/Cas9 knockout in AML cell lines, cell cycle and cytogenetic analysis

    PMID:32197313

    Open questions at the time
    • Molecular basis of premature chromatid separation not defined
    • Single lab, AML-cell-line specific
  10. 2021 Medium

    Established SMARCA5 as a maintainer of chromatin accessibility at lineage-gene promoters, acting with nucleolin to license transcription-factor binding in hematopoiesis.

    Evidence ATAC-seq, RNA-seq, Co-IP (nucleolin) in zebrafish HSPCs

    PMID:32756943

    Open questions at the time
    • Direct biochemical role of nucleolin in remodeling not reconstituted
    • Single lab/model
  11. 2021 Medium

    Generalized the accessibility-licensing model to differentiation programs, showing lncRNA-guided SMARCA5 opens myogenic loci and a developmental requirement in embryos.

    Evidence Co-IP (lncMREF), ATAC-seq, ChIP-seq in muscle satellite cells; siRNA depletion with RNA-seq in mouse/bovine embryos

    PMID:33899080 PMID:36200826

    Open questions at the time
    • How lncRNA guides SMARCA5 to specific loci unresolved
    • Species differences in embryo requirement unexplained
  12. 2021 High

    Provided a clean epistatic chain showing SMARCA5 controls a specific physiological program (RBC homeostasis) via accessibility at the keap1a promoter upstream of Keap1-Nrf2.

    Evidence Zebrafish mutant, ATAC-seq, RNA-seq, keap1a/hmox1a rescue experiments

    PMID:34698638

    Open questions at the time
    • Direct binding of SMARCA5 at keap1a vs broader chromatin effects not distinguished
    • Mammalian conservation of the axis not tested here
  13. 2022 High

    Identified SMARCA5 as a functionally required partner of the NUP98-NSD1 oncofusion, showing its remodeling activity (not condensate assembly) drives leukemic transformation.

    Evidence AP-MS, inducible knockdown, pharmacological inhibition, PLA, FRAP, colony assays in patient cells

    PMID:35073946

    Open questions at the time
    • Specific chromatin targets of the SMARCA5-NUP98-NSD1 module not mapped
    • Mechanism linking remodeling to transformation incomplete
  14. 2022 Medium

    Defined a dosage-dependent requirement for SMARCA5 in restraining senescence and supporting immortalization, telomere maintenance and DNA repair.

    Evidence Conditional single/double-allele deletion, senescence and genotoxic assays, transcriptome and accessibility profiling

    PMID:35269430

    Open questions at the time
    • Direct mechanism of telomere maintenance not established
    • Single lab
  15. 2023 High

    Resolved the core nucleosome-spacing function with temporal precision, showing acute SMARCA5 loss compacts chromatin and abolishes CTCF binding before transcription changes accumulate.

    Evidence Degron degradation in three human cell lines, MNase-seq, nascent transcription, CTCF/H2A.Z ChIP-seq, ATAC-seq

    PMID:36630954

    Open questions at the time
    • How CTCF directs SMARCA5 to specific sites not fully resolved here
    • Downstream transcriptional consequences over longer timescales not profiled
  16. 2024 Medium

    Clarified the DSB recruitment mechanism, showing ACF subunits accumulate independently and via ADP-ribosylation-driven chromatin relaxation rather than direct PAR binding.

    Evidence Live imaging of GFP-tagged subunits, ADP-ribose binding and chromatin relaxation assays

    PMID:38170578

    Open questions at the time
    • Quantitative contribution of relaxation vs other signals not measured
    • Single lab
  17. 2024 Medium

    Identified a post-translational control point, USP3-mediated removal of K63 polyubiquitin, governing SMARCA5 stability and chemoresistance.

    Evidence Co-IP, K63-linkage-specific ubiquitination assays, knockdown/overexpression, docetaxel resistance in vitro and in vivo

    PMID:39500888

    Open questions at the time
    • E3 ligase generating the K63 chains not identified
    • Single lab
  18. 2024 High

    Demonstrated SMARCA5 is required for germinal center formation and B cell activation through transcriptional and accessibility remodeling.

    Evidence Conditional knockout, single-cell multiomics (scRNA + ATAC), ribosomal pull-down, immunization

    PMID:39297882

    Open questions at the time
    • Specific enhancers/promoters mechanistically responsible not isolated
    • Recruitment determinants in activated B cells unknown
  19. 2024 Medium

    Extended SMARCA5's reach to cancer signaling and inflammation through phospho-regulated partner interactions and upstream m6A/ubiquitin control of its levels.

    Evidence Co-IP with PIM1 phospho-SND1 and reporter/xenograft assays (ESCC); DSS UC mouse model with m6A (ALKBH5) and RNF180 ubiquitination assays

    PMID:39060657 PMID:39725102

    Open questions at the time
    • Whether remodeling activity is required for these transcriptional outputs not separated
    • Direct vs indirect roles in each disease context unresolved
  20. 2025 High

    Established SMARCA5 as essential for male meiosis and spermatogenesis, restricting chromatin accessibility in germ cells to enable synapsis, DNA repair and transposon silencing.

    Evidence Germ-cell-specific conditional knockout, scRNA-seq, ATAC-seq, Co-IP with BAZ1A/BAZ2A and repair factors

    PMID:40743397

    Open questions at the time
    • How accessibility restriction is targeted to repeats/promoters not mechanistically resolved
    • Direct role in meiotic recombination machinery not biochemically defined
  21. 2025 Medium

    Proposed a pioneer-factor partnership in which SMARCA5 is recruited by DMRT1 to license retinoic-acid-responsive enhancers for spermatogenic differentiation.

    Evidence Conditional knockout, DMRT1 ChIP-seq, ATAC-seq, Co-IP (preprint)

    PMID:40837621 PMID:41282062

    Open questions at the time
    • Preprint, not peer-reviewed
    • Direct demonstration that SMARCA5 remodeling generates RA-receptor sites needed
  22. 2025 Medium

    Implicated SMARCA5 in cerebellar neural precursor proliferation and SHH-medulloblastoma growth.

    Evidence CRISPR dropout screen, conditional knockout, SHH pathway and in vivo tumor assays

    PMID:40681754

    Open questions at the time
    • Mechanistic link between SMARCA5 remodeling and SHH pathway activation undefined
    • Single lab

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SMARCA5 is selectively targeted to specific genomic loci across its many contexts—and whether its ATPase remodeling activity is required for each transcriptional and disease output—remains unresolved.
  • No unified model for site selection by CTCF, DMRT1, lncRNAs, and cofactor complexes
  • Catalytic dependence not tested for many reported functions
  • No high-resolution structural model of the remodeling reaction in the timeline

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140657 ATP-dependent activity 3 GO:0003677 DNA binding 2 GO:0042393 histone binding 2 GO:0140096 catalytic activity, acting on a protein 2
Localization
GO:0000228 nuclear chromosome 2 GO:0005634 nucleus 2 GO:0005730 nucleolus 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-1640170 Cell Cycle 3 R-HSA-73894 DNA Repair 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-4839726 Chromatin organization 2
Partners
BAZ1ABAZ2ACTCFDMRT1DNMT3BRNF168RSF1USP3
Complex memberships
ACF (SMARCA5-BAZ1A/ACF1)BAZ2A/TIP5 complexRSF (SMARCA5-RSF1)

Evidence

Reading pass · 29 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 SMARCA5/hSNF2H was cloned and identified as a human homologue of Drosophila ISWI, encoding a 1,052 amino-acid protein with a conserved ATPase domain characteristic of the SWI2/SNF2 family, mapped to chromosome 4q31.1→q31.2, suggesting a role in chromatin remodeling. cDNA cloning, sequence homology analysis, Northern blot, FISH mapping Cytogenetics and cell genetics Medium 9730600
2004 SMARCA5/hSNF2H physically interacts with the de novo DNA methyltransferase DNMT3B, as well as HDAC1, HDAC2, HP1 proteins, and Suv39h1; endogenous hSNF2H is associated with DNA methyltransferase activity, co-localizing with DNMT3B in heterochromatic regions. Co-immunoprecipitation, GST pull-down, immunofluorescence co-localization, ATPase activity assay Biochemical and biophysical research communications Medium 15120635
2009 Smarca5 (Snf2h) is localized predominantly to euchromatin, with lesser presence in heterochromatin and nucleoli; Smarca5 heterozygous mice show decreased histone H3 modifications and defects in heterochromatin foci, indicating Smarca5 is a key regulator of global chromatin structure. Confocal microscopy, immunostaining with histone modification markers, heterozygous mouse model Frontiers in bioscience (Elite edition) Medium 19482671
2012 SMARCA5/SNF2H is recruited to DNA double-strand breaks (DSBs) in a PARP1-dependent manner; SMARCA5 and RNF168 interact in a DNA damage- and PARP-dependent manner; RNF168 undergoes poly(ADP-ribosyl)ation after DNA damage, and PAR chains plus RNF168 are required for SMARCA5 binding; SMARCA5 promotes RNF168 accumulation at DSBs to facilitate ubiquitin conjugation and BRCA1 assembly; SMARCA5 depletion renders cells sensitive to IR and causes DSB repair defects. Co-immunoprecipitation, live-cell imaging (recruitment to laser-induced DSBs), siRNA knockdown, IR sensitivity assay, PAR chain functional assays Journal of cell science High 23264744
2014 SMARCA5/SNF2H and its binding partners ACF1 and WSTF are recruited to UV-C-induced DNA damage to facilitate CSB binding and promote transcription recovery after NER; SMARCA5 targeting to UV-C damage depends on transcription, histone modifications, and requires functional SWI2/SNF2-ATPase and SLIDE domains; after initial recruitment, SMARCA5 re-localizes away from the damage center requiring its HAND domain. Live-cell imaging, domain-deletion mutagenesis, UV-C local damage assays, CSB recruitment assay, transcription recovery assay Nucleic acids research High 24990377
2014 SMARCA5 facilitates CTCF binding to its target DNA sites and supports the CTCF enhancer-blocking function at the ICR; SMARCA5 associates with the Cohesin complex and is recruited together with CTCF and Cohesin members to the SPI1 gene -14.4 Enhancer in differentiating myeloid cells, blocking SPI1 (PU.1) expression. ChIP assays, co-immunoprecipitation, reporter/enhancer-blocking assays, AML primary cell analysis PloS one Medium 24498324
2017 Conditional deletion of Smarca5 at the onset of definitive hematopoiesis causes embryonic lethality due to anemia; hematopoietic stem and progenitor cells accumulate but fail to mature into erythroid and myeloid lineages; Smarca5 deficiency increases p53 levels and activates p53 targets, including at residues associated with DNA damage (S15Ph) and CBP/p300 (K376Ac); deletion in committed erythroid cells causes postnatal anemia; ex vivo deletion confirms requirement for erythroid cell proliferation. Conditional knockout mouse models (Vav1-iCre, Epor-iCre, 4-OHT-inducible), hematopoietic phenotyping, Western blot for p53 modifications, flow cytometry Stem cells (Dayton, Ohio) High 28276606
2019 SMARCA5 is required for thymocyte development: conditional knockout causes a developmental block at the DN3 stage of αβ thymocytes and pro-B stage of early B cells; loss leads to massive apoptosis of β-selected DN3 cells, premitotic arrest of DP cells, persistent expression of immature markers (CD44, CD25), and p53 pathway activation; p53 deficiency partially rescues thymus cellularity but not the developmental defects. Conditional knockout mouse model, flow cytometry, gene expression profiling, epistasis with p53 knockout Journal of immunology High 31068388
2020 CRISPR/Cas9-mediated SMARCA5 knockout in AML cell lines inhibits cell cycle progression, induces karyorrhexis and nuclear budding, increases ploidy, and causes premature chromatid separation, indicating a role in mitotic division and chromatid cohesion. CRISPR/Cas9 knockout, cell cycle analysis, cytogenetic analysis, flow cytometry International journal of molecular sciences Medium 32197313
2021 Smarca5 interacts with nucleolin to promote chromatin remodeling in zebrafish fetal hematopoietic stem and progenitor cells, thereby facilitating genomic binding of transcription factors to regulate expression of hematopoietic regulators such as bcl11ab; Smarca5 is responsible for maintenance of chromatin accessibility at promoters of hematopoiesis-related genes. ATAC-seq, RNA-seq, Co-immunoprecipitation (Smarca5-nucleolin interaction), functional assays in zebrafish Blood Medium 32756943
2021 SMARCA5 depletion in mouse preimplantation embryos reduces developmental capability, compromises inner cell mass specification and differentiation (OCT4 not restricted to ICM, reduced NANOG and SOX17), and dysregulates 402 genes at the blastocyst stage; in bovine embryos, depletion does not affect blastocyst development but compromises quality and disrupts primitive endoderm formation (reduced GATA6). siRNA-mediated depletion in mouse and bovine embryos, immunostaining, RNA-seq Biology of reproduction Medium 33899080
2021 The lncRNA lncMREF interacts with Smarca5 to promote chromatin accessibility when muscle satellite cells are activated and differentiate, facilitating genomic binding of p300/CBP/H3K27ac and upregulating myogenic regulators such as MyoD. Co-immunoprecipitation (lncMREF-Smarca5), ATAC-seq, ChIP-seq for H3K27ac/p300, loss-of-function experiments in mouse Nucleic acids research Medium 36200826
2021 In zebrafish, smarca5-deficient red blood cells form blood clots; smarca5 deletion decreases chromatin accessibility at the keap1a promoter and reduces keap1a expression, leading to elevated hmox1a (a downstream target of Keap1-Nrf2 signaling); overexpression of keap1a or knockdown of hmox1a partially rescues blood clot formation, placing smarca5 upstream of the Keap1-Nrf2 pathway in RBC homeostasis. Zebrafish mutant model, ATAC-seq, RNA-seq, drug treatment, rescue experiments (keap1a overexpression, hmox1a knockdown) eLife High 34698638
2022 NUP98-NSD1 oncofusion protein interacts with SMARCA5 (and BPTF) in NUP98-NSD1+ patient cells via the NUP98 FG repeat domains that mediate phase-separated condensate formation; SMARCA5 knockdown or pharmacological inhibition impairs transformation of NUP98-NSD1/FLT3-ITD immortalized hematopoietic cells; SMARCA5 inhibition does not affect condensate formation itself, indicating that SMARCA5 functional activity (not condensate assembly) is required for transformation. Affinity purification-mass spectrometry (AP-MS), inducible knockdown, pharmacological inhibition, proximity ligation assay, FRAP, b-isoxazole condensate assay, methylcellulose colony assay Journal of experimental & clinical cancer research High 35073946
2022 Conditional single- or double-allele Smarca5 deletion in primary mouse cells causes accelerated growth arrest and senescence, increased sensitivity to genotoxic insults, and dramatically decreased capacity to bypass senescence and immortalize; Smarca5 is required for DNA damage repair, telomere maintenance, cell cycle progression, and restriction of apoptosis and senescence. Conditional allele deletion, senescence assays, genotoxic sensitivity assays, transcriptome analysis, chromatin accessibility profiling Cells Medium 35269430
2023 Acute degradation of endogenous SMARCA5 (via degron tag) causes a rapid increase in global nucleosome repeat length (greater chromatin compaction) with few changes in nascent transcription within 6 hours; SMARCA5 is required to control nucleosome repeat length at G1/S and during S phase; 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 binding sites. Degron-tag degradation system in three human cell lines, MNase-seq (nucleosome repeat length), nascent transcription assay, ChIP-seq (CTCF, H2A.Z), ATAC-seq Molecular cell High 36630954
2024 The deubiquitinating enzyme USP3 directly interacts with SMARCA5 and removes K63-linked polyubiquitination of SMARCA5 to maintain its stability; USP3-mediated stabilization of SMARCA5 promotes DNA damage repair and chemotherapy (docetaxel) resistance in prostate cancer cells. Co-immunoprecipitation, ubiquitination assay (K63-linkage specific), siRNA knockdown/overexpression, in vitro and in vivo docetaxel resistance assays Cell death & disease Medium 39500888
2024 Each subunit of the ACF complex (SMARCA5/SNF2H and ACF1/BAZ1A) accumulates at DNA lesions independently of its partner; recruitment of SMARCA5 and ACF1 to damage sites is not due to direct binding to ADP-ribose moieties but is facilitated by ADP-ribosylation-dependent chromatin unfolding/relaxation that permits DNA binding. Live-cell imaging of GFP-tagged proteins at laser-induced damage, ADP-ribose binding assays, chromatin relaxation assays Molecular biology of the cell Medium 38170578
2024 SMARCA5 interaction with SND1 (staphylococcal nuclease domain-containing 1) is potentiated by PIM1-catalyzed phosphorylation of SND1 at serine 426; this SND1-SMARCA5 interaction mediates transcriptional activation of CUX1 in esophageal squamous cell carcinoma; disruption of SND1 S426 phosphorylation impairs the SND1-SMARCA5 interaction and inhibits ESCC tumor growth and metastasis in vivo. Co-immunoprecipitation, phosphorylation assay (PIM1 kinase), siRNA knockdown, reporter assays, in vivo xenograft International journal of biological macromolecules Medium 39725102
2024 ALKBH5 inhibits SMARCA5 expression via m6A modification; RNF180 (E3 ubiquitin ligase) reduces ALKBH5 expression via ubiquitination, thereby de-repressing SMARCA5; elevated SMARCA5 promotes colon inflammation and Th17/Treg imbalance in ulcerative colitis mice. UC mouse model (DSS-induced), siRNA knockdown, flow cytometry (Th17/Treg), m6A modification assay, ubiquitination assay Archives of pharmacal research Medium 39060657
2024 SMARCA5 is required for germinal center (GC) formation; conditional depletion of Smarca5 in B cells does not affect naive B cell compartment but impairs effective proliferation during activation, immunoglobulin class switching, GC formation, and antibody-secreting cell differentiation; single-cell multiomic sequencing shows SMARCA5 is required for transcriptional modifications and genomic accessibility changes at genes supporting B cell activation. Conditional knockout in mice, single-cell multiomic sequencing (scRNA-seq + ATAC-seq), ribosomal pull-down, flow cytometry, immunization experiments The Journal of experimental medicine High 39297882
2024 CTCF recruits SMARCA5 to reposition the CTCF priming nucleosome (CPN) downstream of CTCF binding sites, creating nucleosome-free regions that enhance CTCF occupancy and cohesin stalling; this process requires non-methylated CPNs lacking repressive histone modifications. ChIP-seq, ATAC-seq, MNase-seq, CTCF motif orientation analysis, bioinformatic modeling bioRxivpreprint Low
2025 SMARCA5 interacts with known cofactors BAZ1A/ACF and BAZ2A/TIP5 as well as DNA repair and recombination factors in the testis; germ cell-specific deletion of Smarca5 results in male infertility, meiotic progression failure at pachytene stage, abnormal chromosome synapsis, DNA repair defects, and transposon derepression; SMARCA5 restricts chromatin accessibility in male germ cells at promoters and repeat elements in spermatogonia to guide appropriate chromatin remodeling during meiotic recombination. Conditional knockout mouse (germ cell-specific), scRNA-seq, Co-IP (BAZ1A, BAZ2A, DNA repair factors), ATAC-seq, immunostaining Proceedings of the National Academy of Sciences of the United States of America High 40743397
2025 During the perinatal transition from prospermatogonia to undifferentiated spermatogonia, SMARCA5 is recruited to binding sites of the pioneer transcription factor DMRT1 at distal enhancers and promoters of germline genes; the SMARCA5-DMRT1 pioneer complex establishes chromatin accessibility at these loci, generating poised enhancers/promoters as RA receptor binding sites, thereby licensing transcriptional responses to retinoic acid for spermatogenic differentiation. Germ cell-specific conditional knockout, ChIP-seq (DMRT1), ATAC-seq, Co-IP (SMARCA5-DMRT1), RA signaling assays Research square / bioRxivpreprint Medium 40837621 41282062
2025 Smarca5 knockout in cerebellar granule cell neuron precursors (GCNPs) reduces their proliferative capacity and causes cerebellar hypoplasia; loss of Smarca5 inhibits SHH pathway activation and SHH-medulloblastoma cell proliferation; Smarca5 loss in a Ptch+/- SHH-MB mouse model prolongs survival. CRISPR-Cas9 dropout screen, conditional knockout in mice (GCNPs), proliferation assays, SHH pathway activity assays, in vivo tumor model Scientific reports Medium 40681754
2015 hSNF2H/SMARCA5 interacts with RSF-1 (Rsf complex) in glioma cells; hSNF2H depletion decreases cyclin D1, cyclin E, p-Rb, MMP2, cIAP1, Bcl-2, and phosphorylation of IκBα and p65; changes in cyclin E, Bcl-2, and p-IκBα are not significant upon hSNF2H siRNA treatment in Rsf-1-depleted cells, indicating that hSNF2H regulates NF-κB pathway in an RSF-1-dependent manner. Co-immunoprecipitation, siRNA knockdown, Western blot, MTT/colony assay, Matrigel invasion assay Tumour biology Medium 26666816
2021 RSF1 requires hSNF2H/SMARCA5 and CEBP/β to co-transactivate the IL1B promoter, increasing IL-1β mRNA levels and secretion, thereby driving angiogenesis in myxofibrosarcoma. Co-immunoprecipitation (RSF1-hSNF2H), siRNA knockdown, RT-PCR, reporter assay (IL1B promoter), in vivo xenograft Angiogenesis Medium 33496909
2020 Aberrant (pro)renin receptor [(P)RR] expression upregulates SMARCA5 through a direct molecular interaction, resulting in failure of genomic stability pathways and induction of large numbers of point mutations and structural variations in human pancreatic ductal epithelial cells. Co-immunoprecipitation ((P)RR-SMARCA5), whole genome sequencing, cell transformation assays Communications biology Medium 33247206
2023 SMARCA5 knockdown in hippocampal dentate gyrus impairs contextual fear conditioning memory maintenance and neurogenesis in mice; proteomics analysis reveals SMARCA5 modulates proteins of metabolic pathways (NME3, ACY1) as a mechanism underlying its role in memory. Knockdown via stereotaxic injection, fear conditioning behavioral assay, proteomics analysis, immunostaining Neuroscience bulletin Low 36807260

Source papers

Stage 0 corpus · 68 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Poly(ADP-ribosyl)ation links the chromatin remodeler SMARCA5/SNF2H to RNF168-dependent DNA damage signaling. Journal of cell science 120 23264744
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
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 82 21113140
1998 Cloning and mapping of SMARCA5 encoding hSNF2H, a novel human homologue of Drosophila ISWI. Cytogenetics and cell genetics 68 9730600
2014 Human ISWI complexes are targeted by SMARCA5 ATPase and SLIDE domains to help resolve lesion-stalled transcription. Nucleic acids research 63 24990377
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
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
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 49 25377162
2019 Circ-SMARCA5 suppresses progression of multiple myeloma by targeting miR-767-5p. BMC cancer 48 31601173
2000 Chromatin remodeling gene SMARCA5 is dysregulated in primitive hematopoietic cells of acute leukemia. Leukemia 48 10914549
2022 Long noncoding RNA lncMREF promotes myogenic differentiation and muscle regeneration by interacting with the Smarca5/p300 complex. Nucleic acids research 44 36200826
2017 The ISWI ATPase Smarca5 (Snf2h) Is Required for Proliferation and Differentiation of Hematopoietic Stem and Progenitor Cells. Stem cells (Dayton, Ohio) 42 28276606
2023 Human SMARCA5 is continuously required to maintain nucleosome spacing. Molecular cell 40 36630954
2011 SMARCA5 methylation and expression in gastric cancer. Cancer investigation 39 21261476
2020 Circular RNA SMARCA5 may serve as a tumor suppressor in non-small cell lung cancer. Journal of clinical laboratory analysis 38 31944395
2022 SMARCA5 interacts with NUP98-NSD1 oncofusion protein and sustains hematopoietic cells transformation. Journal of experimental & clinical cancer research : CR 31 35073946
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
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) 31 23778407
2021 Smarca5-mediated epigenetic programming facilitates fetal HSPC development in vertebrates. Blood 30 32756943
2014 Epigenetic control of SPI1 gene by CTCF and ISWI ATPase SMARCA5. PloS one 30 24498324
2020 Nm23-H1 inhibits lung cancer bone-specific metastasis by upregulating miR-660-5p targeted SMARCA5. Thoracic cancer 28 32022430
2021 Circ SMARCA5 Inhibited Tumor Metastasis by Interacting with SND1 and Downregulating the YWHAB Gene in Cervical Cancer. Cell transplantation 26 33588586
2021 Circular RNA SMARCA5 functions as an anti-tumor candidate in colon cancer by sponging microRNA-552. Cell cycle (Georgetown, Tex.) 24 33749508
2020 Circular RNA SMARCA5 suppressed non-small cell lung cancer progression by regulating miR-670-5p/RBM24 axis. Acta biochimica et biophysica Sinica 23 33085761
2017 gga-miR-99a targets SMARCA5 to regulate Mycoplasma gallisepticum (HS strain) infection by depressing cell proliferation in chicken. Gene 23 28652181
2020 MicroRNA miR-100 Decreases Glioblastoma Growth by Targeting SMARCA5 and ErbB3 in Tumor-Initiating Cells. Technology in cancer research & treatment 22 32945237
2020 A Novel miR-146a-POU3F2/SMARCA5 Pathway Regulates Stemness and Therapeutic Response in Glioblastoma. Molecular cancer research : MCR 21 32973101
2020 Loss of ISWI ATPase SMARCA5 (SNF2H) in Acute Myeloid Leukemia Cells Inhibits Proliferation and Chromatid Cohesion. International journal of molecular sciences 20 32197313
2016 miR-151-5p, targeting chromatin remodeler SMARCA5, as a marker for the BRCAness phenotype. Oncotarget 20 27385001
2022 Chromatin Remodeler Smarca5 Is Required for Cancer-Related Processes of Primary Cell Fitness and Immortalization. Cells 19 35269430
2020 MiR-146b-5p suppresses the malignancy of GSC/MSC fusion cells by targeting SMARCA5. Aging 19 32632040
2024 E3 ubiquitin ligase RNF180 mediates the ALKBH5/SMARCA5 axis to promote colon inflammation and Th17/Treg imbalance in ulcerative colitis mice. Archives of pharmacal research 17 39060657
2022 MicroRNA-182-5p aggravates ulcerative colitis by inactivating the Wnt/β-catenin signaling pathway through DNMT3A-mediated SMARCA5 methylation. Genomics 16 35378241
2019 Circular RNA SMARCA5 is overexpressed and promotes cell proliferation, migration as well as invasion while inhibits cell apoptosis in bladder cancer. Translational cancer research 16 35116915
2019 Circular RNA SMARCA5 inhibits gastric cancer progression through targeting the miR-346/ FBXL2 axis. RSC advances 16 35515212
2013 Beyond the binding site: in vivo identification of tbx2, smarca5 and wnt5b as molecular targets of CNBP during embryonic development. PloS one 16 23667590
2021 Functional roles of the chromatin remodeler SMARCA5 in mouse and bovine preimplantation embryos†. Biology of reproduction 14 33899080
2015 Overexpression of hSNF2H in glioma promotes cell proliferation, invasion, and chemoresistance through its interaction with Rsf-1. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 14 26666816
2024 USP3 promotes DNA damage response and chemotherapy resistance through stabilizing and deubiquitinating SMARCA5 in prostate cancer. Cell death & disease 13 39500888
2020 Long non-coding RNA HAGLROS facilitates the malignant phenotypes of NSCLC cells via repressing miR-100 and up-regulating SMARCA5. Biomedical journal 13 35307327
2019 ISWI ATPase Smarca5 Regulates Differentiation of Thymocytes Undergoing β-Selection. Journal of immunology (Baltimore, Md. : 1950) 13 31068388
1999 Nickel(II) acetate-treated Chinese hamster ovary cells differentially express Vimentin, hSNF2H homologue, and H ferritin. Biochemical and biophysical research communications 13 10329430
2021 The chromatin-remodeling enzyme Smarca5 regulates erythrocyte aggregation via Keap1-Nrf2 signaling. eLife 12 34698638
2023 Expression status of circ-SMARCA5, circ-NOL10, circ-LDLRAD3, and circ-RHOT1 in patients with colorectal cancer. Scientific reports 10 37587156
2023 Circular RNA SMARCA5 inhibits cholangiocarcinoma via microRNA-95-3p/tumor necrosis factor receptor associated factor 3 axis. Anti-cancer drugs 9 36727735
2021 RSF1 requires CEBP/β and hSNF2H to promote IL-1β-mediated angiogenesis: the clinical and therapeutic relevance of RSF1 overexpression and amplification in myxofibrosarcomas. Angiogenesis 9 33496909
2023 The miR-100-5p Targets SMARCA5 to Regulate the Apoptosis and Intracellular Survival of BCG in Infected THP-1 Cells. Cells 7 36766816
2020 Aberrant (pro)renin receptor expression induces genomic instability in pancreatic ductal adenocarcinoma through upregulation of SMARCA5/SNF2H. Communications biology 7 33247206
2023 Chromatin Remodeling Factor SMARCA5 is Essential for Hippocampal Memory Maintenance via Metabolic Pathways in Mice. Neuroscience bulletin 6 36807260
2025 SMARCA5 restricts chromatin accessibility to promote male meiosis and fertility in mammals. Proceedings of the National Academy of Sciences of the United States of America 5 40743397
2024 The recruitment of ACF1 and SMARCA5 to DNA lesions relies on ADP-ribosylation dependent chromatin unfolding. Molecular biology of the cell 4 38170578
2024 SND1-SMARCA5 interaction strengthened by PIM promotes the proliferation, metastasis, and chemoresistance of esophageal squamous cell carcinoma. International journal of biological macromolecules 4 39725102
2023 Hyperglycemia-Suppressed SMARCA5 Disrupts Transcriptional Homeostasis to Facilitate Endothelial Dysfunction in Diabetes. Diabetes & metabolism journal 4 36872061
2009 Nuclear localization of ISWI ATPase Smarca5 (Snf2h) in mouse. Frontiers in bioscience (Elite edition) 4 19482671
2024 Evaluation of Circular RNA SMARCA5 as a Novel Biomarker for Hepatocellular Carcinoma. Asian Pacific journal of cancer prevention : APJCP 3 38680002
2024 Differential requirements for Smarca5 expression during hematopoietic stem cell commitment. Communications biology 2 38424235
2023 Circular RNA SMARCA5 Modulates Epithelial-Mesenchymal Transformation, Proliferation, and Metastasis of Nasopharyngeal Carcinoma Cells via microRNA-582-3p/Phosphatase and Tensin Homolog Axis. Evidence-based complementary and alternative medicine : eCAM 2 36686977
2025 The SMARCA5-DMRT1 Pioneer Complex Establishes Epigenetic Priming to Direct Male Germline Development. Research square 1 41282062
2024 SMARCA5-mediated chromatin remodeling is required for germinal center formation. The Journal of experimental medicine 1 39297882
2021 Circular RNA SMARCA5 Inhibits the Proliferation, Migration, and Invasion of Non-Small Cell Lung Cancer by miR-19b-3p/HOXA9 Axis [Retraction]. OncoTargets and therapy 1 34848969
2026 RSF-1/hSNF2H Promotes the Proliferation and Migration of Adenoid Cystic Cancer Cells. Bulletin of experimental biology and medicine 0 41949721
2026 RETRACTION: Circular RNA SMARCA5 May Serve as a Tumor Suppressor in Non-Small Cell Lung Cancer. Journal of clinical laboratory analysis 0 41972935
2025 SMARCA5 is required for the development of granule cell neuron precursors and Sonic Hedgehog Medulloblastoma growth. Scientific reports 0 40681754
2025 The SMARCA5-DMRT1 Pioneer Complex Establishes Epigenetic Priming to Direct Male Germline Development. bioRxiv : the preprint server for biology 0 40837621
2024 The chromatin remodeler SMARCA5 binds to d-block metal supports: Characterization of affinities by IMAC chromatography and QM analysis. PloS one 0 39374200
2023 Till SMARCA5 loss do nucleosomes part. Molecular cell 0 36804911
2023 Retracted: Circular RNA SMARCA5 Modulates Epithelial-Mesenchymal Transformation, Proliferation, and Metastasis of Nasopharyngeal Carcinoma Cells via microRNA-582-3p/Phosphatase and Tensin Homolog Axis. Evidence-based complementary and alternative medicine : eCAM 0 38125158

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