Affinage

SMARCE1

SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily E member 1 · UniProt Q969G3

Length
411 aa
Mass
46.6 kDa
Annotated
2026-04-28
61 papers in source corpus 24 papers cited in narrative 24 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMARCE1 (BAF57) is a core structural subunit of the mammalian SWI/SNF (BAF) chromatin-remodeling complex that stabilizes the canonical BAF (cBAF) core–ATPase module interaction, maintains proper subunit stoichiometry, and directs the complex to specific genomic loci to regulate chromatin accessibility and nucleosome stability (PMID:35681054, PMID:38357971, PMID:20460533). Its HMG domain binds four-way junction DNA, and SMARCE1 serves as a platform for transcription factor recruitment—directly interacting with AR, ERα, HIF1A, MYCN, and FoxO3a to mediate their target gene activation or repression, thereby controlling hormone-dependent proliferation, apoptosis, and metastatic gene programs (PMID:15743818, PMID:16769725, PMID:27495308, PMID:35978151, PMID:33010889). SMARCE1 also functions outside the SWI/SNF complex, forming a complex with the transcription factor ILF3 to drive protease expression and invasive behavior, and interacting with splicing factor SRSF1 to regulate Cyclin D1 alternative splicing (PMID:28377514, PMID:33670012). Loss of SMARCE1 destabilizes cBAF complexes on chromatin—reducing enhancer accessibility and creating a therapeutically targetable dependency on ncBAF—a mechanism underlying clear cell meningioma pathogenesis (PMID:35681054).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2002 Low

    Whether BAF57 has roles beyond SWI/SNF housekeeping in patterning was unknown; Xenopus XBaf57 cooperated with Smad7 to promote neural marker expression in ectodermal explants, providing the first evidence that BAF57 participates in lineage-specific transcriptional decisions during embryonic development.

    Evidence Expression cloning and ectodermal explant assays in Xenopus

    PMID:12128220

    Open questions at the time
    • Overexpression assay without loss-of-function confirmation
    • No direct binding to Smad7 or target promoters demonstrated
    • Xenopus ortholog, not confirmed in mammalian systems
  2. 2005 High

    How SWI/SNF complexes are recruited to nuclear hormone receptor target genes was unclear; BAF57 was shown to directly bind the androgen receptor and ERα, and its depletion abolished hormone-dependent transactivation and proliferation, establishing BAF57 as a required bridge between nuclear hormone receptors and SWI/SNF chromatin remodeling.

    Evidence Co-IP, ChIP, siRNA knockdown and rescue in prostate and breast cancer cells

    PMID:15743818 PMID:16769725

    Open questions at the time
    • Structural basis of BAF57–receptor interaction unresolved
    • Selectivity for ERα over ERβ mechanism unknown
  3. 2005 High

    How SWI/SNF subunit stoichiometry is maintained was not understood; BAF155/BAF170 were shown to directly stabilize BAF57 protein levels, with unincorporated BAF57 degraded by the proteasome, establishing a quality-control mechanism for complex assembly.

    Evidence Co-IP, deletion mapping, proteasome inhibitor assays

    PMID:16199878

    Open questions at the time
    • Ubiquitin ligase responsible for BAF57 degradation not identified
    • Whether this mechanism operates for all peripheral subunits unclear
  4. 2005 High

    Whether BAF57 had direct transcriptional targets linked to apoptosis was unknown; BAF57 was found to occupy the CYLD promoter and activate its transcription, with CYLD required for BAF57-mediated cell death, connecting SWI/SNF activity to a specific tumor-suppressive effector.

    Evidence ChIP, microarray, siRNA rescue in cancer cell lines

    PMID:16135788

    Open questions at the time
    • Whether BAF57 alone is sufficient or requires specific SWI/SNF subcomplexes at the CYLD locus not tested
  5. 2010 High

    How BAF57 affects SWI/SNF complex composition and cell cycle progression was undefined; quantitative proteomics of purified SWI/SNF from BAF57-depleted cells revealed selective loss of BAF180, G2-M accumulation, and misregulation of late G2 genes, demonstrating that BAF57 is essential for proper subunit composition and cell cycle transit.

    Evidence SILAC-based proteomics of SWI/SNF, cell cycle analysis, colony formation in cancer cells

    PMID:20460533

    Open questions at the time
    • Mechanism by which BAF57 retains BAF180 within the complex not defined
    • Whether BAF180 loss is the sole cause of G2-M arrest unclear
  6. 2015 Medium

    How SMARCE1 influences receptor tyrosine kinase signaling was unknown; SMARCE1 was shown to occupy the EGFR locus and suppress EGFR transcription through regulation of Polycomb component CBX2, linking SMARCE1 loss to EGFR upregulation and resistance to MET/ALK inhibitors in lung cancer.

    Evidence ChIP, siRNA, drug sensitivity assays in NSCLC cells

    PMID:25656847

    Open questions at the time
    • Direct mechanism connecting CBX2 regulation to EGFR repression not fully delineated
    • Whether this pathway operates outside NSCLC untested
  7. 2016 High

    The mechanism of SMARCE1's pro-survival function during anchorage-independent conditions was uncharacterized; SMARCE1 was found to interact with HIF1A to activate PTK2/FAK, suppressing BIM and protecting against anoikis, thereby promoting lung metastasis.

    Evidence Co-IP, ChIP, xenograft models, anoikis assays in breast cancer

    PMID:27495308

    Open questions at the time
    • Whether the SMARCE1–HIF1A interaction occurs within or outside the SWI/SNF complex not resolved
  8. 2017 High

    Whether SMARCE1 could function independently of SWI/SNF was an open question; SMARCE1 was shown to form a SWI/SNF-independent complex with ILF3 that drives secreted protease expression and basement membrane invasion, establishing a non-canonical function for this subunit.

    Evidence Co-IP, primary human tissue invasion assays, xenograft metastasis models

    PMID:28377514

    Open questions at the time
    • Stoichiometry and full composition of the SMARCE1–ILF3 complex unknown
    • How SMARCE1 is partitioned between SWI/SNF-dependent and -independent pools unclear
  9. 2020 High

    The structural basis of BAF57's DNA-binding mode was unknown; the crystal structure of the HMG domain at 2.55 Å revealed an L-shaped three-helix fold that binds four-way junction DNA with ~296 nM affinity, providing the first atomic-resolution view of how BAF57 engages non-B-form DNA.

    Evidence X-ray crystallography, fluorescence quenching binding assay

    PMID:33010889

    Open questions at the time
    • No structure of the HMG domain bound to DNA
    • Relevance of 4WJ binding to in vivo genomic targeting not demonstrated
  10. 2022 High

    How SMARCE1 loss rewires chromatin remodeling complex identity was a central unanswered question; biochemical and genomic profiling of SMARCE1-deficient clear cell meningioma cells showed that SMARCE1 stabilizes the cBAF core–ATPase module, and its loss shifts the balance toward ncBAF, creating a pharmacologically exploitable ncBAF dependency.

    Evidence Biochemical complex purification, ATAC-seq, ChIP-seq, ncBAF inhibitor assays in patient-derived cells

    PMID:35681054

    Open questions at the time
    • Structural basis for SMARCE1 selectivity toward cBAF over ncBAF unknown
    • Whether ncBAF dependency generalizes beyond clear cell meningioma untested in vivo
  11. 2022 Medium

    Direct structural contacts between SMARCE1 and other BAF core subunits lacked atomic detail; a binary SMARCE1(210-284)–SMARCC1(862-966) crystal was obtained at 3.2 Å, and ternary/tetrameric BAF subcomplexes were successfully reconstituted, defining the minimal interaction surfaces.

    Evidence Co-expression, co-purification, X-ray crystallography

    PMID:35158202

    Open questions at the time
    • Full structure not yet refined and published
    • Functional consequences of disrupting this interface not tested
  12. 2024 Medium

    Whether SMARCE1 influences nucleosome stability genome-wide was not established; disruption in mouse ESCs revealed loosened histone-DNA binding, ectopic SWI/SNF distribution, and impaired heterochromatin formation during differentiation, showing that SMARCE1 is essential for both nucleosome stability and lineage-specific chromatin compaction.

    Evidence ESC gene disruption, sucrose gradient sedimentation, histone binding assays, chromatin accessibility profiling, differentiation assays

    PMID:38357971

    Open questions at the time
    • Mechanism by which SMARCE1 tightens histone-DNA contacts not defined
    • Whether effects are cBAF-specific or involve other subcomplexes not resolved
  13. 2025 Medium

    How SMARCE1 controls organ-specific proliferation was explored in vivo; zebrafish smarce1 mutants showed ventricular cardiomyocyte hyperproliferation rescued by mRNA re-expression, and this was mechanistically linked to increased chromatin accessibility at Stat3 signaling loci, establishing a Smarce1–Stat3 proliferation-restraining axis in heart development.

    Evidence ENU mutagenesis, morpholino, mRNA rescue, ATAC-seq, scRNA-seq, Stat3 genetic/pharmacological epistasis in zebrafish

    PMID:40950410 PMID:41808150

    Open questions at the time
    • Whether the Smarce1–Stat3 axis operates in mammalian cardiomyocytes unknown
    • Direct binding of Smarce1 to Stat3 loci not shown by ChIP

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: (1) how SMARCE1 is partitioned between SWI/SNF-dependent and SWI/SNF-independent roles, (2) the structural basis for cBAF selectivity over ncBAF, and (3) whether the ncBAF dependency created by SMARCE1 loss is therapeutically viable across tumor types beyond clear cell meningioma.
  • No full-length SMARCE1 structure in the context of the intact BAF complex
  • In vivo therapeutic window for ncBAF inhibition in SMARCE1-deficient tumors not established
  • Mechanism governing SMARCE1 allocation to SWI/SNF-independent complexes unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0005198 structural molecule activity 5 GO:0003677 DNA binding 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 5 GO:0005694 chromosome 3
Pathway
R-HSA-74160 Gene expression (Transcription) 6 R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 3 R-HSA-162582 Signal Transduction 2 R-HSA-1640170 Cell Cycle 2 R-HSA-5357801 Programmed Cell Death 2
Partners
ARESR1HIF1AILF3MYCNSMARCC1SMARCC2SRSF1
Complex memberships
SMARCE1–ILF3 complexSWI/SNF (BAF/cBAF)

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2005 BAF57/SMARCE1 directly binds to the androgen receptor (AR) and is recruited to endogenous AR target genes upon ligand activation; loss of BAF57 severely compromises AR-dependent transactivation and AR-dependent proliferation in prostatic adenocarcinoma cells, and this action depends on SWI/SNF ATPase function. Co-immunoprecipitation, chromatin immunoprecipitation, siRNA knockdown, rescue experiments, proliferation assays Molecular and cellular biology High 15743818
2005 BAF155 and BAF170 regulate the cellular levels of BAF57/SMARCE1 through direct protein-protein interactions; excess BAF57 that cannot bind BAF155/170 is degraded via proteasome-dependent proteolysis, maintaining stoichiometric levels of SWI/SNF subunits. Co-immunoprecipitation, deletion mapping, proteasome inhibitor assays, exogenous expression of deletion mutants Molecular and cellular biology High 16199878
2005 BAF57/SMARCE1 induces apoptosis by directly activating expression of the tumor suppressor CYLD; CYLD is a direct transcriptional target of BAF57 as demonstrated by chromatin immunoprecipitation, and suppression of CYLD blocks BAF57-mediated cell death. Stable cell line expression, microarray analysis, chromatin immunoprecipitation, siRNA knockdown of CYLD Molecular and cellular biology High 16135788
2006 BAF57/SMARCE1 is required for ERα-mediated transcription and estrogen-stimulated proliferation in breast cancer cells; structure-function analysis defined a region within the ERα hinge domain essential for BAF57 recruitment, and BAF57 selectively regulates ERα but not ERβ. siRNA knockdown, dominant-negative expression, structure-function analysis, reporter assays, proliferation assays The Journal of biological chemistry High 16769725
2008 BAF57/SMARCE1 is recruited to the AR DNA-binding domain/hinge region upon receptor activation; a BAF57-derived inhibitory peptide (BIPep) blocks AR residence on chromatin and inhibits androgen-dependent prostate cancer cell proliferation. Chromatin immunoprecipitation, peptide inhibitor assays, cell proliferation assays Cancer research High 18559499
2009 Neuron-specific alternative splicing of exons II, III, and IV in BAF57/SMARCE1 generates N-terminally truncated isoforms (N-BAF57s) that associate with Brg1, Brm, BAF155, and BAF170 into functional SWI/SNF complexes in neurons and regulate NRSE-containing genes. RT-PCR, biochemical fractionation, co-immunoprecipitation, transient overexpression with gene expression analysis Journal of neurochemistry Medium 19245665
2010 BAF57/SMARCE1 depletion by shRNA causes co-depletion of BAF180 from the SWI/SNF complex (without reducing total BAF180), G2-M cell cycle accumulation, inhibition of colony formation, and transcriptional misregulation of late G2 cell cycle genes; BAF57 is required for proper SWI/SNF subunit composition. Stable shRNA knockdown, quantitative SILAC-based proteomics of purified SWI/SNF complex, cell proliferation and colony formation assays, cell cycle analysis Cancer research High 20460533
2013 Aberrant BAF57/SMARCE1 overexpression in prostate cancer bypasses androgen signaling, induces α2 integrin upregulation via altered SWI/SNF complex occupancy at the α2 integrin locus, and confers a prometastatic migratory advantage blocked by anti-α2 integrin antibody. Immunohistochemistry on clinical specimens, gene expression analysis, ChIP, cell migration assays, antibody blockade Clinical cancer research Medium 23493350
2015 SMARCE1 binds to regulatory regions of the EGFR locus to suppress EGFR transcription, in part through regulating expression of the Polycomb Repressive Complex component CBX2; SMARCE1 loss induces EGFR expression and confers resistance to MET and ALK inhibitors in NSCLC. ChIP, siRNA knockdown, gene expression analysis, drug sensitivity assays Cell research Medium 25656847
2016 SMARCE1 interacts with HIF1A and potentiates its transcriptional activity in response to loss of attachment, leading to rapid PTK2 (FAK) activation; both HIF1A and PTK2 are required for SMARCE1-mediated protection against anoikis and lung metastasis through ERK/AKT activation and BIM suppression. Co-immunoprecipitation, ChIP, siRNA knockdown, xenograft mouse models, anoikis assays, immunoblotting Breast cancer research : BCR High 27495308
2017 SMARCE1 drives invasive progression of DCIS by forming a SWI/SNF-independent complex with transcription factor ILF3 to regulate expression of secreted proteases that degrade basement membrane; SMARCE1 is required for invasion within primary human mammary tissues and for metastasis in vivo. Co-immunoprecipitation, siRNA/shRNA knockdown, primary human mammary tissue invasion assays, xenograft metastasis models Proceedings of the National Academy of Sciences of the United States of America High 28377514
2018 In zebrafish, smarce1 loss-of-function causes defects in endocardial development and misshapen heart tube; Smarce1 binds to cis-regulatory regions of the gata5 gene and is necessary for BAF complex recruitment to these regions. CRISPR/Cas9 mutagenesis in zebrafish, gene expression analysis, ChIP Scientific reports Medium 30337622
2020 FoxO3a requires BAF57/SMARCE1 (upregulated in the 6-OHDA Parkinson's disease model) to induce PUMA transcription; BAF57 knockdown blocks FoxO3a-dependent PUMA induction and protects dopaminergic neurons from 6-OHDA toxicity. siRNA knockdown, Western blot, neuronal cell culture and primary dopaminergic neuron models, RNAi-mediated silencing Journal of neurochemistry Medium 31971251
2020 Crystal structure of the HMG domain of BAF57/SMARCE1 resolved at 2.55 Å reveals three α-helices in an L-shaped conformation stabilized by a hydrophobic core; the domain binds four-way junction DNA with 295.83 nM affinity, and the 4WJ DNA binding site was identified. X-ray crystallography, fluorescence quenching assay Biochemical and biophysical research communications High 33010889
2021 BAF57/SMARCE1 interacts with splicing factor SRSF1 and regulates mechanical stress-induced alternative splicing of Cyclin D1 to generate the cyclin D1b isoform; overexpression and knockdown experiments confirm BAF57 as a critical regulator of this splicing event. Co-immunoprecipitation, RT-PCR, siRNA knockdown, overexpression in stretched osteoblast and keratinocyte cells Genes Medium 33670012
2022 SMARCE1 plays a structural role in selectively stabilizing the canonical BAF (cBAF) complex core-ATPase module interaction; loss of SMARCE1 in clear cell meningioma causes cBAF complexes to fail to stabilize on chromatin, reduces enhancer accessibility, and increases formation of ncBAF complexes; SMARCE1-deficient cells are hypersensitive to ncBAF inhibition. Biochemical complex purification, ATAC-seq, ChIP-seq, small-molecule ncBAF inhibitor assays, transcriptomic profiling in patient-derived CCM cells Nature genetics High 35681054
2022 SMARCE1 directly interacts with MYCN and is required for MYCN-mediated transcriptional activation of downstream targets (PLK1, ODC1, E2F2) in neuroblastoma; MYCN also directly regulates SMARCE1 transcription through a non-canonical E-box in its promoter. Co-immunoprecipitation, ChIP, siRNA knockdown, rescue overexpression, colony formation and tumorigenicity assays Oncogene Medium 35978151
2022 SMARCE1 (aa 210-284) directly interacts with SMARCC1 (BAF155, aa 862-966); co-expression of SMARCC1/SMARCE1 binary, SMARCC1/SMARCD1/SMARCE1 ternary, and SMARCC1/SMARCD1/SMARCB1/SMARCE1 tetrameric complexes was achieved; crystal diffraction data of the SMARCC1/SMARCE1 binary complex was obtained at 3.2 Å. Co-expression, co-purification, X-ray crystallography Biochemical and biophysical research communications Medium 35158202
2024 Disruption of Smarce1 in mouse embryonic stem cells causes dissociation of other SWI/SNF components from the complex, loosened histone-DNA binding (decreased nucleosome stability), ectopic genomic distribution of the SWI/SNF complex, and impaired heterochromatin formation during differentiation. ESC gene disruption, sucrose gradient sedimentation, histone binding assays, ATAC-seq equivalent chromatin analysis, differentiation assays Journal of cell science Medium 38357971
2025 In zebrafish, loss of smarce1 function causes ventricular cardiomyocyte hyperproliferation without hypertrophy, while smarce1 overexpression reduces cardiomyocyte proliferation; mRNA rescue normalizes the phenotype, establishing smarce1 as a cell-autonomous negative regulator of cardiomyocyte proliferation during heart development. ENU mutagenesis screen, morpholino knockdown, mRNA rescue, Tet-On myocardium-specific overexpression, EdU labeling, immunofluorescence Frontiers in cell and developmental biology Medium 40950410
2026 In zebrafish, Smarce1 deficiency enhances cardiomyocyte proliferation by modulating chromatin accessibility and regulating the transcriptional landscape of Stat3 signaling components; genetic and pharmacological inhibition of Stat3 suppresses Smarce1-dependent cardiomyocyte hyperproliferation, establishing a Smarce1-Stat3 axis. Loss-of-function genetics, RNA-seq, single-cell RNA-seq, ATAC-seq, Stat3 pharmacological inhibition, genetic epistasis Biological research Medium 41808150
2007 SMARCE1 binds directly to the HBV core promoter containing naturally occurring deletions (identified by gel shift assay and DNA-protein array) and represses HBV replication and promoter activity. Gel shift assay, DNA-protein array, promoter activity assays, replication assays Biochimica et biophysica acta Medium 17669635
2006 A biallelic frameshift mutation in BAF57/SMARCE1 in BT549 breast cancer cells produces a truncated protein that loses the ability to bind ERα but retains binding to SRC1e; expression of truncated BAF57 abnormally increases SRC1e coactivation of ERα. Genomic DNA and cDNA sequencing, co-immunoprecipitation, transcriptional reporter assays Breast cancer research and treatment Medium 16538531
2002 Xenopus BAF57 co-operates with XSmad7 to increase expression of neural markers in ectodermal explants; XBaf57 is expressed in ectoderm and pre-involuting mesoderm during gastrulation and in CNS during neurulation, implicating BAF57-containing SWI/SNF complexes in neural induction. Expression cloning, ectodermal explant assays, in situ hybridization Mechanisms of development Low 12128220

Source papers

Stage 0 corpus · 61 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Loss-of-function mutations in SMARCE1 cause an inherited disorder of multiple spinal meningiomas. Nature genetics 200 23377182
2014 Genotype-phenotype correlation of Coffin-Siris syndrome caused by mutations in SMARCB1, SMARCA4, SMARCE1, and ARID1A. American journal of medical genetics. Part C, Seminars in medical genetics 132 25168959
2014 Germline SMARCE1 mutations predispose to both spinal and cranial clear cell meningiomas. The Journal of pathology 107 25143307
2005 Regulating SWI/SNF subunit levels via protein-protein interactions and proteasomal degradation: BAF155 and BAF170 limit expression of BAF57. Molecular and cellular biology 106 16199878
2005 BAF57 governs androgen receptor action and androgen-dependent proliferation through SWI/SNF. Molecular and cellular biology 98 15743818
2006 The SWI/SNF chromatin remodeling subunit BAF57 is a critical regulator of estrogen receptor function in breast cancer cells. The Journal of biological chemistry 80 16769725
2005 The BRG1- and hBRM-associated factor BAF57 induces apoptosis by stimulating expression of the cylindromatosis tumor suppressor gene. Molecular and cellular biology 65 16135788
2008 Targeting the BAF57 SWI/SNF subunit in prostate cancer: a novel platform to control androgen receptor activity. Cancer research 63 18559499
2017 Loss of SMARCE1 expression is a specific diagnostic marker of clear cell meningioma: a comprehensive immunophenotypical and molecular analysis. Brain pathology (Zurich, Switzerland) 59 28474749
2020 Clear cell meningiomas are defined by a highly distinct DNA methylation profile and mutations in SMARCE1. Acta neuropathologica 49 33319313
2016 A heritable form of SMARCE1-related meningiomas with important implications for follow-up and family screening. Neurogenetics 47 26803492
2016 SMARCE1 regulates metastatic potential of breast cancer cells through the HIF1A/PTK2 pathway. Breast cancer research : BCR 39 27495308
2015 SMARCE1 suppresses EGFR expression and controls responses to MET and ALK inhibitors in lung cancer. Cell research 36 25656847
2010 A role for BAF57 in cell cycle-dependent transcriptional regulation by the SWI/SNF chromatin remodeling complex. Cancer research 36 20460533
2022 SMARCE1 deficiency generates a targetable mSWI/SNF dependency in clear cell meningioma. Nature genetics 35 35681054
2017 SMARCE1 is required for the invasive progression of in situ cancers. Proceedings of the National Academy of Sciences of the United States of America 35 28377514
2015 SMARCE1 mutations in pediatric clear cell meningioma: case report. Journal of neurosurgery. Pediatrics 29 26114992
2013 Aberrant BAF57 signaling facilitates prometastatic phenotypes. Clinical cancer research : an official journal of the American Association for Cancer Research 29 23493350
2009 N-terminally truncated BAF57 isoforms contribute to the diversity of SWI/SNF complexes in neurons. Journal of neurochemistry 28 19245665
2010 Tau deficiency leads to the upregulation of BAF-57, a protein involved in neuron-specific gene repression. FEBS letters 26 20338169
2017 SMARCE1 mutation screening in classification of clear cell meningiomas. Histopathology 25 27891692
2014 Pediatric intracranial clear cell meningioma associated with a germline mutation of SMARCE1: a novel case. Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery 25 25249420
2020 Forkhead Box O3a requires BAF57, a subunit of chromatin remodeler SWI/SNF complex for induction of p53 up-regulated modulator of apoptosis (Puma) in a model of Parkinson's disease. Journal of neurochemistry 24 31971251
2019 MicroRNA-802 induces hepatitis B virus replication and replication through regulating SMARCE1 expression in hepatocellular carcinoma. Cell death & disease 24 31611549
2006 Identification of BAF57 mutations in human breast cancer cell lines. Breast cancer research and treatment 21 16538531
2016 SMARCE1, a rare cause of Coffin-Siris Syndrome: Clinical description of three additional cases. American journal of medical genetics. Part A 19 27264197
2016 The developmental and pathogenic roles of BAF57, a special subunit of the BAF chromatin-remodeling complex. FEBS letters 18 27149204
2022 WTAP mediates FOXP3 mRNA stability to promote SMARCE1 expression and augment glycolysis in colon adenocarcinoma. Mammalian genome : official journal of the International Mammalian Genome Society 16 36173464
2021 BAF57/SMARCE1 Interacting with Splicing Factor SRSF1 Regulates Mechanical Stress-Induced Alternative Splicing of Cyclin D1. Genes 16 33670012
2014 Overexpression of SMARCE1 is associated with CD8+ T-cell infiltration in early stage ovarian cancer. The international journal of biochemistry & cell biology 16 24880093
2015 Expression of BAF57 in ovarian cancer cells and drug sensitivity. Cancer science 15 25611552
2017 miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma. World journal of gastroenterology 14 28740345
2018 smarce1 mutants have a defective endocardium and an increased expression of cardiac transcription factors in zebrafish. Scientific reports 13 30337622
2022 SMARCE1 promotes neuroblastoma tumorigenesis through assisting MYCN-mediated transcriptional activation. Oncogene 12 35978151
2011 Identification and characterization of novel potentially oncogenic mutations in the human BAF57 gene in a breast cancer patient. Breast cancer research and treatment 10 21465167
1999 Cloning, chromosomal location, and expression analysis of murine Smarce1-related, a new member of the high-mobility 365 group gene family. Genomics 10 10486208
2020 Long noncoding RNA HOTTIP promotes the metastatic potential of ovarian cancer through the regulation of the miR-615-3p/SMARCE1 pathway. The Kaohsiung journal of medical sciences 9 32783402
2020 The importance of genetic counseling and screening for people with pathogenic SMARCE1 variants: A family study. American journal of medical genetics. Part A 9 33185983
2007 Cellular transcription modulator SMARCE1 binds to HBV core promoter containing naturally occurring deletions and represses viral replication. Biochimica et biophysica acta 9 17669635
2002 Cloning and developmental expression of Baf57 in Xenopus laevis. Mechanisms of development 8 12128220
2023 SMARCA4 and SMARCE1 in gastric cancer: Correlation with ARID1A, and microsatellite stability, and SMARCE1/ERBB2 co-amplification. Cancer medicine 7 36916408
2012 SMARCE1 Promotes chicken embryonic gonad development by regulating ER α and AR expression. Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation 6 22584849
2020 Anaplastic Astrocytoma in a Child With Coffin-Siris Syndrome and a Germline SMARCE1 Mutation: A Case Report. Journal of pediatric hematology/oncology 5 30499906
2020 Pediatric clear cell meningioma involving the middle cranial fossa in the context of NF2 and SMARCE1 mutations. Annals of diagnostic pathology 5 32311644
2022 Assembly and interaction of core subunits of BAF complexes and crystal study of the SMARCC1/SMARCE1 binary complex. Biochemical and biophysical research communications 4 35158202
2020 Crystal structure of the HMG domain of human BAF57 and its interaction with four-way junction DNA. Biochemical and biophysical research communications 4 33010889
2018 Identification of a de novo splicing variant in the Coffin-Siris gene, SMARCE1, in a patient with Angelman-like syndrome. Molecular genetics & genomic medicine 4 30548424
2025 Smarce1 fine-tunes cardiomyocyte proliferation in the embryonic zebrafish heart. Frontiers in cell and developmental biology 2 40950410
2024 Mutation of the SWI/SNF complex component Smarce1 decreases nucleosome stability in embryonic stem cells and impairs differentiation. Journal of cell science 2 38357971
2023 Mother and daughter with a SMARCE1 mutation resulting in a cervical clear cell meningioma at an identical location: illustrative cases. Journal of neurosurgery. Case lessons 2 36593672
2023 SMARCE1-related meningiomas: A clear example of cancer predisposing syndrome. European journal of medical genetics 2 37164167
2021 Smarce1 and Tensin 4 Are Putative Modulators of Corneoscleral Stiffness. Frontiers in bioengineering and biotechnology 2 33634081
2020 The Potential Tumor Promotional Role of circVAPA in Retinoblastoma via Regulating miR-615-3p and SMARCE1. OncoTargets and therapy 2 32848418
2019 SMARCE1-related Coffin-Siris Syndrome: Case report and otolaryngologic manifestations of the syndrome. International journal of pediatric otorhinolaryngology 2 31675646
2018 Immuno-suppressive function of nucleus-transducible BAF57-ΔPH in T cell activation via degradation of endogenous BAF57. International journal of hematology 2 29978433
2021 BAF57 Is a Potential Determinant of Colorectal Cancer Malignancy. Anticancer research 1 34732413
2020 [The role of SMARCE1 in the diagnosis of clear cell meningioma]. Zhonghua bing li xue za zhi = Chinese journal of pathology 1 32187894
2026 Thoracic chordoma following intracranial meningioma in a patient with a novel germline SMARCE1 variant. European journal of medical genetics 0 41547400
2026 Coptisine alleviates insulin resistance by suppressing SMARCE1-mediated glycolysis. Biochemical and biophysical research communications 0 41662796
2026 Smarce1-dependent modulation of Stat3 signaling governs cardiomyocyte proliferation. Biological research 0 41808150
2025 The Smarce1 subunit of the BAF complex performs distinct, stage-specific functions during zebrafish retinal development. Neuroscience 0 41052624