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
2026-06-10
61 papers in source corpus 26 papers cited in narrative 26 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMARCE1 (BAF57) is an integral subunit of mammalian SWI/SNF (BAF) chromatin-remodeling complexes that stabilizes complex architecture and couples remodeling activity to specific transcriptional programs (PMID:35681054, PMID:38357971). It performs a structural role by stabilizing the canonical BAF core-ATPase interaction; its loss destabilizes cBAF on chromatin, reduces enhancer accessibility, and shifts the balance toward BRD9-containing ncBAF complexes, sensitizing cells to ncBAF inhibition (PMID:35681054). SMARCE1 is required for proper subunit stoichiometry — its depletion co-depletes BAF180 from the complex — and is itself regulated by proteasomal degradation governed by the levels of its direct partners BAF155 (SMARCC1) and BAF170, with the SMARCE1–SMARCC1 interface mapped structurally and biochemically (PMID:16199878, PMID:20460533, PMID:35158202, PMID:29978433). Through its HMG domain, which binds four-way-junction DNA, and through direct contacts with sequence-specific factors, SMARCE1 serves as an adapter that recruits SWI/SNF to defined loci, including direct binding of the androgen receptor DNA-binding/hinge region and the ERα hinge to enable ligand-activated transcription (PMID:15743818, PMID:18559499, PMID:16769725, PMID:33010889). It governs cell-cycle progression and transcription of cell-cycle and developmental genes (PMID:20460533), and additionally acts within SWI/SNF-independent complexes — for example with ILF3 to drive basement-membrane invasion and with HIF1A to suppress anoikis — implicating it in cancer cell migration and metastasis (PMID:28377514, PMID:27495308). Germline heterozygous loss-of-function mutations in SMARCE1 cause familial multiple spinal clear-cell meningiomas through a tumor-suppressor two-hit mechanism with loss of protein in tumors (PMID:23377182), whereas somatic truncation in breast cancer can yield gain-of-function effects, such as a truncated protein that loses ERα binding but retains and potentiates SRC1e coactivation (PMID:16538531).

Mechanistic history

Synthesis pass · year-by-year structured walk · 26 steps
  1. 2002 Low

    Established an early developmental role for BAF57 by showing it cooperates with a signaling effector to promote a tissue fate, hinting at chromatin remodeling in patterning before its complex role was defined.

    Evidence Expression cloning and ectodermal explant assays in Xenopus identifying XBaf57 as an XSmad7 modulator

    PMID:12128220

    Open questions at the time
    • Single overexpression explant assay without mechanistic placement
    • No demonstration of endogenous requirement
    • Mammalian relevance not addressed
  2. 2005 High

    Defined SMARCE1 as a direct adapter linking SWI/SNF to nuclear hormone receptor signaling, answering how a remodeler is targeted to hormone-responsive genes.

    Evidence Co-IP, ChIP on endogenous AR targets, siRNA knockdown and proliferation assays in prostate cancer cells

    PMID:15743818

    Open questions at the time
    • Precise AR contact surface not yet mapped
    • Generality across other receptors untested at this stage
  3. 2005 High

    Showed BAF57 abundance is set by its core partners and proteasomal turnover, establishing how complex stoichiometry is enforced post-translationally.

    Evidence Exogenous expression, proteasome inhibition, Co-IP and deletion mapping of BAF57–BAF155 interaction

    PMID:16199878

    Open questions at the time
    • Responsible E3 ligase not identified
    • Whether degradation regulates complex assembly dynamically unaddressed
  4. 2005 High

    Demonstrated tumor-suppressor activity by restoring BAF57 in deficient breast cells and identifying a direct pro-apoptotic transcriptional target.

    Evidence Stable re-expression, growth/apoptosis assays, microarray, ChIP and siRNA epistasis on CYLD

    PMID:16135788

    Open questions at the time
    • Breadth of the BAF57 target gene program beyond CYLD unresolved
    • Mechanism of CYLD-dependent death not detailed
  5. 2006 High

    Extended the adapter model to ERα and defined receptor-subtype selectivity, mapping the ERα hinge as the recruitment determinant.

    Evidence siRNA knockdown, reporter assays and structure-function deletion mapping in breast cancer cells

    PMID:16769725

    Open questions at the time
    • Structural basis of hinge recognition not resolved
    • Why ERβ is not engaged unexplained
  6. 2006 Medium

    Revealed a potential gain-of-function route in cancer: a truncating mutation that uncouples ERα binding from coactivator engagement.

    Evidence Sequencing of BT549 mutation, Co-IP for ER and SRC1e binding, reporter assays

    PMID:16538531

    Open questions at the time
    • In vivo oncogenic consequence not established
    • Single cell line context
  7. 2007 Medium

    Identified a direct DNA-binding, gene-repressive activity by showing SMARCE1 binds and represses a viral promoter.

    Evidence EMSA, DNA-protein array and overexpression replication assay on HBV core promoter

    PMID:17669635

    Open questions at the time
    • Whether repression requires the SWI/SNF complex unclear
    • Single lab functional validation
  8. 2008 High

    Mapped the AR recruitment domain and showed it is pharmacologically actionable, demonstrating a BAF57-derived peptide blocks AR chromatin residence.

    Evidence ChIP recruitment mapping and BIPep functional blockade in AR-positive prostate cancer cells

    PMID:18559499

    Open questions at the time
    • Structural detail of the BAF57–AR interface not resolved
    • Specificity of peptide for AR vs other receptors not tested
  9. 2009 Medium

    Showed tissue-specific isoform diversity by characterizing neuron-enriched N-terminally truncated BAF57 isoforms that still assemble into SWI/SNF.

    Evidence RT-PCR, fractionation, Co-IP with Brg1/Brm/BAF155/BAF170 and overexpression effects on NRSE genes

    PMID:19245665

    Open questions at the time
    • Endogenous functional role of isoforms in neurons untested
    • Single lab
  10. 2010 High

    Established SMARCE1 as required for SWI/SNF subunit composition and cell-cycle progression, linking complex integrity to G2-M control.

    Evidence SILAC quantitative proteomics of purified SWI/SNF, shRNA knockdown, cell cycle and colony formation assays

    PMID:20460533

    Open questions at the time
    • Direct cell-cycle gene targets not fully enumerated
    • Mechanism of selective BAF180 co-depletion unclear
  11. 2013 High

    Defined disease causation: germline loss-of-function establishes SMARCE1 as a tumor suppressor for familial clear-cell meningioma via a two-hit mechanism.

    Evidence Exome and Sanger sequencing in families plus IHC for protein loss in tumors

    PMID:23377182

    Open questions at the time
    • Molecular driver linking SMARCE1 loss to clear-cell histology not yet defined here
    • Second-hit events not enumerated
  12. 2013 Medium

    Showed elevated SMARCE1 can be pro-oncogenic, redirecting SWI/SNF occupancy to drive integrin-dependent prostate cancer migration.

    Evidence Expression analysis, ChIP at α2 integrin locus, migration assays and antibody blockade

    PMID:23493350

    Open questions at the time
    • Single lab study
    • Mechanism of altered SWI/SNF locus targeting unresolved
  13. 2015 High

    Connected SMARCE1 loss to therapy resistance by showing it represses EGFR transcription via CBX2 regulation.

    Evidence ChIP at EGFR locus, siRNA knockdown, drug-resistance and rescue assays in NSCLC

    PMID:25656847

    Open questions at the time
    • Direct vs CBX2-mediated repression contributions not separated
    • Generality across other RTKs untested
  14. 2016 High

    Identified a SWI/SNF-independent anoikis-protective axis through SMARCE1 potentiation of HIF1A and downstream FAK/ERK/AKT signaling.

    Evidence Co-IP, ChIP, siRNA epistasis with HIF1A and PTK2, xenograft lung metastasis model

    PMID:27495308

    Open questions at the time
    • Whether the HIF1A interaction is fully SWI/SNF-independent not exhaustively shown
    • Direct target genes mediating survival not detailed
  15. 2017 High

    Demonstrated a SWI/SNF-independent invasion mechanism via a SMARCE1–ILF3 complex driving protease expression and metastasis.

    Evidence Knockdown, primary mammary tissue invasion assay, Co-IP and in vivo xenograft metastasis

    PMID:28377514

    Open questions at the time
    • Structural basis of the ILF3 interaction unknown
    • Which proteases are direct transcriptional targets not fully resolved
  16. 2018 High

    Defined an in vivo developmental requirement, showing Smarce1 directs BAF recruitment to gata5 regulatory regions during cardiac/endocardial development.

    Evidence CRISPR knockout zebrafish, expression analysis and ChIP at gata5 locus

    PMID:30337622

    Open questions at the time
    • Direct target gene network beyond gata5 not mapped
    • Conservation to mammalian heart development not tested here
  17. 2018 Medium

    Showed a peptide disrupting the BAF155–BAF57 interface destabilizes both subunits and is immunomodulatory in vivo, reinforcing the stoichiometric dependency.

    Evidence Nucleus-transducible ntBAF57-ΔPH fragment, Co-IP, T cell assays and in vivo sepsis model

    PMID:29978433

    Open questions at the time
    • Mechanism of T cell suppression downstream of complex destabilization unclear
    • Single lab
  18. 2020 High

    Solved the HMG domain structure and quantified its four-way-junction DNA binding, providing a structural basis for SMARCE1's intrinsic DNA-recognition activity.

    Evidence X-ray crystallography at 2.55 Å and fluorescence quenching binding assay

    PMID:33010889

    Open questions at the time
    • Role of 4WJ binding in vivo not established
    • Full-length protein structure unresolved
  19. 2020 Medium

    Implicated SMARCE1 in neuronal apoptosis by showing it is required for FoxO3a-driven PUMA induction in a Parkinson's disease model.

    Evidence siRNA knockdown, qPCR/Western, primary neurons and PC12 cells, in vivo 6-OHDA rat model

    PMID:31971251

    Open questions at the time
    • Whether SMARCE1 acts through SWI/SNF at the PUMA locus not shown
    • Single lab
  20. 2021 Low

    Linked SMARCE1 to stress-responsive alternative splicing through interaction with SRSF1 and control of cyclin D1 isoform choice.

    Evidence Co-IP with SRSF1, RT-PCR, knockdown/overexpression under mechanical stretch

    PMID:33670012

    Open questions at the time
    • Single Co-IP without reciprocal/structural validation
    • Direct role in splice-site selection mechanism untested
  21. 2022 High

    Provided the mechanistic explanation for clear-cell meningioma: SMARCE1 selectively stabilizes cBAF, and its loss rebalances toward ncBAF, creating a targetable dependency.

    Evidence Biochemical fractionation, ATAC-seq, genetic loss-of-function and ncBAF small-molecule inhibition in CCM cells and tumors

    PMID:35681054

    Open questions at the time
    • Direct molecular contact stabilizing the core-ATPase module not structurally resolved
    • Why CCM tissue is uniquely sensitive not fully explained
  22. 2022 Medium

    Defined a feed-forward oncogenic loop in neuroblastoma where SMARCE1 enables MYCN target activation and MYCN drives SMARCE1 transcription.

    Evidence Co-IP, ChIP at MYCN targets and the SMARCE1 promoter, knockdown and rescue, reporter assays

    PMID:35978151

    Open questions at the time
    • Structural basis of the SMARCE1–MYCN interaction unknown
    • Single lab study
  23. 2022 Medium

    Mapped the core-assembly interface biochemically, localizing the SMARCE1 region that engages SMARCC1 and reconstituting tetrameric core subcomplexes.

    Evidence Co-expression/co-purification, pulldown fragment mapping and crystallization (3.2 Å) of the SMARCC1/SMARCE1 binary complex

    PMID:35158202

    Open questions at the time
    • Limited resolution and functional validation
    • How the interface controls in-cell complex integrity not shown
  24. 2024 High

    Established that Smarce1 is required for nucleosome stability and complex integrity, linking its loss to impaired heterochromatin formation during differentiation.

    Evidence Homozygous mutant mouse ESCs, sucrose gradient sedimentation, histone-binding and differentiation assays

    PMID:38357971

    Open questions at the time
    • Molecular basis of altered nucleosome stability unresolved
    • Which differentiation genes are directly affected not enumerated
  25. 2025 High

    Identified Smarce1 as a cell-autonomous negative regulator of cardiomyocyte proliferation during heart development using converging genetic approaches.

    Evidence ENU mutant, morpholino, mRNA rescue and myocardium-specific overexpression with EdU proliferation readout in zebrafish

    PMID:40950410

    Open questions at the time
    • Direct transcriptional targets controlling proliferation not yet defined here
    • Mammalian relevance untested
  26. 2026 High

    Resolved the downstream effector of cardiomyocyte proliferation control by defining a Smarce1–Stat3 axis acting through chromatin accessibility and cell-cycle dynamics.

    Evidence RNA-seq, scRNA-seq, ATAC-seq with genetic loss-of-function and pharmacological Stat3 modulation in zebrafish

    PMID:41808150

    Open questions at the time
    • Direct Smarce1 occupancy at Stat3 pathway loci not shown
    • Conservation in mammalian cardiac regeneration untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SMARCE1 mechanistically achieves locus selectivity — switching between SWI/SNF-dependent stabilization and SWI/SNF-independent partnerships (ILF3, HIF1A, SRSF1) — and the structural basis of its sequence-specific factor contacts remain unresolved.
  • No full-length structure of SMARCE1 within an assembled BAF complex
  • Determinants choosing SWI/SNF-dependent vs -independent complexes unknown
  • Genome-wide direct target map integrating contexts lacking

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 5 GO:0140110 transcription regulator activity 5 GO:0003677 DNA binding 3 GO:0005198 structural molecule activity 3 GO:0003723 RNA binding 1
Localization
GO:0005634 nucleus 3 GO:0000228 nuclear chromosome 2
Pathway
R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1266738 Developmental Biology 4 R-HSA-162582 Signal Transduction 3 R-HSA-1640170 Cell Cycle 3 R-HSA-1643685 Disease 2 R-HSA-4839726 Chromatin organization 2
Partners
ARESR1HIF1AILF3MYCNSMARCC1SMARCC2SRSF1
Complex memberships
SMARCE1-ILF3 complexcBAF (canonical SWI/SNF)ncBAF (BRD9-containing)

Evidence

Reading pass · 26 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2022 SMARCE1 plays a structural role in selectively stabilizing the canonical BAF (cBAF) complex core-ATPase module interaction. In SMARCE1-deficient clear cell meningioma cells, cBAF complexes fail to stabilize on chromatin, reducing enhancer accessibility, and residual core module components increase formation of BRD9-containing non-canonical BAF (ncBAF) complexes. This combined attenuation of cBAF and increased ncBAF activity generates the CCM-specific gene expression signature, and SMARCE1-deficient cells exhibit heightened sensitivity to small-molecule ncBAF inhibition. Biochemical fractionation, chromatin accessibility assays (ATAC-seq), small-molecule inhibition, genetic loss-of-function in CCM cell lines and patient tumors Nature genetics High 35681054
2005 BAF57/SMARCE1 directly binds to the androgen receptor (AR) and is recruited to endogenous AR target loci upon ligand activation. Loss of BAF57 severely compromises AR-dependent transactivation in prostatic adenocarcinoma cells, and this activity requires SWI/SNF ATPase function. Both BAF57 and BRM are required for AR-dependent proliferation of prostate cancer cells. Co-immunoprecipitation, chromatin immunoprecipitation (ChIP), siRNA knockdown, reporter assays, cell proliferation assays Molecular and cellular biology High 15743818
2008 BAF57/SMARCE1 is recruited to the AR DNA-binding domain/hinge region concomitant with receptor activation. A BAF57-derived inhibitory peptide (BIPep) blocks AR residence on chromatin and AR-dependent gene activation, inhibiting androgen-dependent prostate cancer cell proliferation in AR-positive cells. ChIP, peptide inhibitor functional assays, cell proliferation assays Cancer research High 18559499
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 as essential for BAF57 recruitment. BAF57 is an ER subtype-selective modulator, specifically regulating ERα- but not ERβ-mediated transcription. siRNA knockdown, reporter assays, structure-function deletion analysis, cell proliferation assays The Journal of biological chemistry High 16769725
2005 Exogenous expression of BAF57/SMARCE1 or certain deletion mutants triggers proteasome-dependent degradation of endogenous BAF57. The protein levels of BAF155 and BAF170 dictate the maximum cellular amount of BAF57 through direct protein-protein interactions; specific interacting domains between BAF57 and BAF155 were mapped. Exogenous expression, proteasome inhibitor experiments, co-immunoprecipitation, deletion mapping Molecular and cellular biology High 16199878
2005 Re-expression of BAF57/SMARCE1 in BT549 breast carcinoma cells (which lack endogenous BAF57) induces growth arrest, contact inhibition, and apoptosis. ChIP analysis identified CYLD (familial cylindromatosis tumor suppressor) as a direct transcriptional target of BAF57. siRNA suppression of CYLD inhibited BAF57-mediated cell death. Stable cell line re-expression, growth assays, microarray, ChIP, siRNA knockdown Molecular and cellular biology High 16135788
2010 Depletion of BAF57 from the SWI/SNF complex causes significant co-depletion of BAF180 from the complex without reducing total cellular BAF180 levels, establishing BAF57 as required for maintaining proper SWI/SNF subunit composition. BAF57 knockdown causes G2-M accumulation, inhibition of colony formation, and transcriptional misregulation of cell cycle genes involved in late G2. SILAC-based quantitative proteomics of affinity-purified SWI/SNF, shRNA knockdown, cell cycle analysis, colony formation assay Cancer research High 20460533
2017 SMARCE1 drives invasion of ductal carcinoma in situ (DCIS) by regulating expression of secreted proteases that degrade basement membrane. SMARCE1 forms a SWI/SNF-independent complex with transcription factor ILF3 to promote invasion. SMARCE1 is also required for metastasis in vivo in xenograft models. siRNA/shRNA knockdown, primary human mammary tissue invasion assay, in vivo xenograft metastasis, co-immunoprecipitation Proceedings of the National Academy of Sciences of the United States of America High 28377514
2016 SMARCE1 interacts with and potentiates the transcriptional activity of HIF1A in response to loss of attachment (anoikis conditions). This leads to rapid PTK2 (FAK) activation and downstream ERK/AKT pathway activation, suppressing pro-apoptotic BIM. Both HIF1A and PTK2 are required for SMARCE1-mediated protection against anoikis and lung metastasis in vivo. Co-immunoprecipitation, ChIP, siRNA knockdown, xenograft metastasis model, ERK/AKT signaling assays Breast cancer research : BCR High 27495308
2015 SMARCE1 binds to regulatory regions of the EGFR locus and suppresses EGFR transcription, in part through regulating expression of Polycomb Repressive Complex component CBX2. SMARCE1 loss induces EGFR expression and confers resistance to MET and ALK inhibitors in non-small cell lung cancers. ChIP, siRNA knockdown, drug resistance assays, gene expression analysis Cell research High 25656847
2013 Heterozygous germline loss-of-function mutations in SMARCE1 cause familial multiple spinal meningiomas. Tumors from affected individuals show loss of SMARCE1 protein expression, consistent with a tumor suppressor two-hit mechanism. All mutation-associated tumors were of clear-cell histological subtype. Exome sequencing, Sanger sequencing, immunohistochemistry for SMARCE1 protein loss Nature genetics High 23377182
2013 Aberrant elevated BAF57/SMARCE1 expression in prostate cancer circumvents androgen-mediated signaling, induces α2 integrin upregulation via altered SWI/SNF occupancy at the α2 integrin locus, and confers a pro-metastatic migratory advantage that is attenuated by anti-α2 integrin antibody blockade. Gene expression analysis, ChIP at α2 integrin locus, cell migration assays, antibody blockade, immunohistochemistry of human specimens Clinical cancer research Medium 23493350
2009 Neuron-specific alternative splicing of BAF57/SMARCE1 exons II, III, and IV produces N-terminally truncated isoforms (N-BAF57s) predominantly expressed in the nervous system. These isoforms associate with Brg1, Brm, BAF155, and BAF170 into functional SWI/SNF complexes, and their overexpression in non-neural cells affects expression of NRSE-containing genes. RT-PCR, biochemical fractionation, co-immunoprecipitation, transient overexpression Journal of neurochemistry Medium 19245665
2020 BAF57/SMARCE1 is upregulated in a Parkinson's disease model (6-OHDA) and is required for induction of the pro-apoptotic protein PUMA by FoxO3a in dopaminergic neurons. BAF57 is necessary for FoxO3a-mediated transcriptional activation of PUMA, linking SWI/SNF chromatin remodeling to neuronal apoptosis in this context. siRNA knockdown, qPCR, Western blot, primary neuronal cultures and PC12 cells, in vivo 6-OHDA rat model Journal of neurochemistry Medium 31971251
2022 SMARCE1 directly interacts with MYCN and is required for MYCN-mediated transcriptional activation of downstream target genes (PLK1, ODC1, E2F2) in neuroblastoma cells. Conversely, MYCN directly regulates SMARCE1 transcription through binding to a non-canonical E-box in the SMARCE1 promoter, creating a positive feedback loop. Co-immunoprecipitation, ChIP, siRNA knockdown, overexpression rescue, promoter reporter assays Oncogene Medium 35978151
2020 Crystal structure of the HMG domain of BAF57/SMARCE1 was solved at 2.55 Å resolution. The domain consists of three α-helices in an L-shaped form stabilized by a hydrophobic core. Fluorescence quenching assays showed that BAF57-HMG binds four-way junction (4WJ) DNA with an affinity of ~296 nM, and the 4WJ DNA-binding site was identified structurally. X-ray crystallography, fluorescence quenching binding assay Biochemical and biophysical research communications High 33010889
2022 The assembly mechanism of BAF core subunits was investigated; SMARCE1 (residues 210-284) interacts with SMARCC1 (residues 862-966). Binary, ternary, and tetrameric complexes of SMARCC1/SMARCD1/SMARCB1/SMARCE1 were reconstituted, and crystals of the SMARCC1(883-966)/SMARCE1(210-284) binary complex were obtained with diffraction data to 3.2 Å. Co-expression and co-purification, crystallography (3.2 Å), pulldown mapping of interacting fragments Biochemical and biophysical research communications Medium 35158202
2024 Disruption of Smarce1 in mouse embryonic stem cells (ESCs) causes dissociation of other SWI/SNF complex components, decreased nucleosome stability (loosened histone-DNA binding), and ectopic genomic redistribution of the SWI/SNF complex as shown by sucrose gradient sedimentation. Unstable nucleosomes persist during differentiation, impairing heterochromatin formation required for normal ESC differentiation. Homozygous mutant ESC generation, sucrose gradient sedimentation, histone binding assays, differentiation assays Journal of cell science High 38357971
2018 Loss of smarce1 in zebrafish causes defects in endocardial development from early stages, leading to a misshapen heart tube and increased expression of cardiac transcription factors. Smarce1 binds to cis-regulatory regions of the gata5 gene and is necessary for recruitment of the BAF complex to these regions. CRISPR/Cas9 knockout zebrafish, gene expression analysis, ChIP at gata5 locus Scientific reports High 30337622
2025 Loss of smarce1 function in zebrafish (ENU mutant and morpholino knockdown) causes ventricular cardiomyocyte hyperproliferation without hypertrophy, while myocardium-specific overexpression reduces CM proliferation. Exogenous smarce1 mRNA injection rescues the hyperproliferative phenotype, establishing smarce1 as a cell-autonomous negative regulator of CM 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 High 40950410
2026 Smarce1 deficiency in zebrafish enhances cardiomyocyte proliferative activity by modulating cell cycle dynamics and chromatin accessibility. Integrative transcriptomic and epigenomic analysis revealed that Smarce1 regulates Stat3 signaling components. Genetic and pharmacological modulation of Stat3 confirmed its functional contribution to Smarce1-dependent CM proliferation, establishing a Smarce1-Stat3 axis in cardiac growth. RNA-seq, single-cell RNA-seq, ATAC-seq, genetic Smarce1 loss-of-function, pharmacological Stat3 modulation Biological research High 41808150
2007 SMARCE1 binds directly to an HBV core promoter containing naturally occurring deletions, as demonstrated by gel shift assay and DNA-protein array. SMARCE1 overexpression represses HBV replication, demonstrating a direct functional role as a host repressor of HBV. Gel shift assay (EMSA), DNA-protein array, overexpression functional assay Biochimica et biophysica acta Medium 17669635
2021 BAF57/SMARCE1 interacts with splicing factor SRSF1 (as shown by co-immunoprecipitation), and mechanical stress-induced alternative splicing of cyclin D1 (producing cyclin D1b isoform) is regulated by BAF57/SMARCE1 in osteoblast and keratinocyte cell lines. Co-immunoprecipitation, RT-PCR, overexpression and siRNA knockdown, cyclic stretch mechanical stimulation Genes Low 33670012
2018 A nucleus-transducible BAF57 fragment lacking proline-rich and HMG domains (ntBAF57-ΔPH) disrupts the interaction between BAF155 and BAF57, leading to proteasomal degradation of endogenous BAF57 and BAF155, and suppresses T cell activation. In vivo administration enhanced survival in sepsis-induced mice. Protein transduction into CD4+ T cells, co-immunoprecipitation, gene expression analysis, in vivo sepsis model International journal of hematology Medium 29978433
2006 A biallelic frameshift mutation in BAF57/SMARCE1 exon 5 in BT549 breast cancer cells produces a truncated protein that has lost the ability to bind ERα but retains binding to nuclear receptor coactivator SRC1e. Expression of this truncated BAF57 increases SRC1e coactivation of ERα, suggesting gain-of-function oncogenic properties. Genomic DNA/cDNA sequencing, co-immunoprecipitation (ER binding and SRC1e binding), reporter assays Breast cancer research and treatment Medium 16538531
2002 Xenopus BAF57 (XBaf57) was isolated via expression cloning as a modulator of XSmad7. XBaf57 cooperates with XSmad7 to increase expression of neural markers in ectodermal explants, suggesting a role in neural induction. Expression cloning, ectodermal explant assay, 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 201 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 133 25168959
2014 Germline SMARCE1 mutations predispose to both spinal and cranial clear cell meningiomas. The Journal of pathology 108 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) 60 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 48 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
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 25 31971251
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
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
2021 BAF57/SMARCE1 Interacting with Splicing Factor SRSF1 Regulates Mechanical Stress-Induced Alternative Splicing of Cyclin D1. Genes 17 33670012
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
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
2017 miR-29a promotes hepatitis B virus replication and expression by targeting SMARCE1 in hepatoma carcinoma. World journal of gastroenterology 15 28740345
2015 Expression of BAF57 in ovarian cancer cells and drug sensitivity. Cancer science 15 25611552
2018 smarce1 mutants have a defective endocardium and an increased expression of cardiac transcription factors in zebrafish. Scientific reports 14 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

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