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Showing SMARCC1 — BAF155 is a alias.

SMARCC1

SWI/SNF complex subunit SMARCC1 · UniProt Q92922

Length
1105 aa
Mass
122.9 kDa
Annotated
2026-06-10
64 papers in source corpus 44 papers cited in narrative 44 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

SMARCC1 (BAF155/SRG3) is a core scaffold subunit of the mammalian SWI/SNF (BAF) chromatin remodeling complex that builds and stabilizes the complex, controls chromatin accessibility at lineage- and signal-responsive enhancers, and thereby governs development, tumor suppression, and inflammatory gene programs (PMID:9151708, PMID:17255092, PMID:39088321). It directly assembles the BAF core through its SWIRM domain binding SNF5/SMARCB1, its SANT domain binding BRG1, and additional contacts with BAF60a and BAF57/SMARCE1, and these interactions protect partner subunits from proteasomal degradation, including by competitively blocking the CHFR E3 ligase (PMID:17255092, PMID:22285184, PMID:28438634, PMID:32244797, PMID:35158202). Its own abundance is tightly regulated: RNF138 mediates K48-linked polyubiquitination at Lys643 to fine-tune chromatin remodeling at inflammatory loci, Wwp2 targets SMARCC1 via a WW-PPPY interaction for degradation, and RBM15/METTL3-dependent m6A methylation destabilizes its mRNA (PMID:36800290, PMID:24365151, PMID:31020615). CARM1/PRMT4 methylates SMARCC1 at arginine R1064, redirecting the complex to super-enhancer-associated oncogenes through BRD4 recruitment while repressing interferon pathway genes and coupling the complex to RNA-processing factors to control nascent transcription (PMID:24434208, PMID:34865122, PMID:42239058). Functionally, SMARCC1 establishes accessible chromatin required for hematopoietic priming, cortical neurogenesis, and oligodendrocyte differentiation, acts in the p53/p21 tumor-suppressor axis and as a suppressor of PI3K/AKT signaling, and modulates the activities of transcription factors including the glucocorticoid receptor, androgen receptor, PAX6, HIF-1α, and JUND (PMID:20935679, PMID:39088321, PMID:30240734, PMID:41423560, PMID:34249931, PMID:11441086, PMID:15923603, PMID:37478146). Patient SMARCC1 variants in defined domains fail to rescue Xenopus phenotypes, establishing SMARCC1 as causative in human hydrocephalus (PMID:38128548).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1997 Medium

    Established SMARCC1 as a physical component of the mammalian SWI/SNF complex and assigned it a concrete cellular function in glucocorticoid-induced apoptosis, moving it from an uncharacterized gene to a SWI/SNF subunit with a phenotype.

    Evidence Co-immunoprecipitation with BRG1 and antisense knockdown apoptosis assay in S49.1 thymoma cells

    PMID:9151708

    Open questions at the time
    • Did not define which domains mediate complex assembly
    • Mechanism linking SWI/SNF to apoptotic gene programs not resolved
  2. 2001 High

    Knockout and dominant-negative studies showed SMARCC1 is essential for early embryogenesis and neural tube closure, and that it forms a complex with the glucocorticoid receptor to confer GC apoptotic sensitivity, tying chromatin remodeling to nuclear receptor signaling and development.

    Evidence Srg3 null mice, blastocyst outgrowth, transgenic overexpression and dominant-negative GR co-IP/apoptosis assays

    PMID:11441086 PMID:11604513

    Open questions at the time
    • Target genes of the SRG3-GR complex not identified
    • Molecular basis of the neural tube closure defect unresolved
  3. 2004 Medium

    A series of promoter studies defined how SMARCC1 expression is itself transcriptionally controlled (Notch1/Deltex1, TCR-Ras/MEK/ERK via Id3, E2A/HEB, Sp1, nitric oxide), establishing SMARCC1 dosage as the rheostat that sets thymocyte glucocorticoid sensitivity.

    Evidence Promoter reporter assays, ChIP, EMSA, pharmacological inhibitors and transgenic rescue in thymocytes

    PMID:11504912 PMID:15016814 PMID:15016815 PMID:15187086 PMID:16288722 PMID:16341126

    Open questions at the time
    • These map upstream regulation, not SMARCC1's own chromatin targets
    • Single-lab promoter-centric system
  4. 2005 Medium

    Demonstrated that SMARCC1 stabilizes BAF subunits (BAF57) against proteasomal degradation and can act as an AR coactivator independently of BRG1/BRM, revealing both a structural scaffold role and a complex-independent transcriptional function.

    Evidence Co-IP, deletion mapping, proteasome inhibition, and ChIP/reporter assays in BRG1/BRM-deficient cells

    PMID:15923603 PMID:16199878

    Open questions at the time
    • Generality of BRG1-independent activity to other transcription factors unknown
    • Stoichiometry of subunit stabilization not quantified
  5. 2007 High

    Domain-mapped the SMARCC1 interactions with SNF5 (SWIRM), BRG1 (SANT), and BAF60a and showed these contacts attenuate partner degradation in vivo, defining SMARCC1 as the assembly hub that maintains BAF complex integrity.

    Evidence Co-IP, domain-deletion mutagenesis and proteasome inhibition in transgenic and haploinsufficient mouse cells

    PMID:17255092

    Open questions at the time
    • Did not resolve atomic interfaces
    • Did not address whether stabilization is competitive with E3 ligases
  6. 2010 High

    Placed SMARCC1 in the p53/p21 tumor-suppressor pathway by showing its loss promotes G1 arrest, antagonizes DNA-damage apoptosis, and that heterozygous mice are tumor-prone, establishing tumor-suppressor function.

    Evidence Knockout/heterozygous mouse tumor incidence, western blot and cell cycle analysis

    PMID:20935679

    Open questions at the time
    • Direct chromatin targets driving p53/p21 induction not identified
    • Mechanism of p53-dependent SMARCC1 degradation unclear
  7. 2012 Medium

    Identified CHFR and Wwp2 E3 ligases as opposing forces on BAF stability and SMARCC1 turnover, showing SMARCC1 protects subunits by blocking CHFR while being itself a Wwp2 ubiquitination substrate, refining the degradation logic of the complex.

    Evidence Co-IP, ubiquitination assays, catalytic-dead mutant and proteasome inhibition

    PMID:22285184 PMID:24365151

    Open questions at the time
    • Physiological signals controlling CHFR/Wwp2 activity unknown
    • Single-lab biochemistry without in vivo loss-of-function
  8. 2014 High

    Discovered CARM1-dependent methylation of SMARCC1 at R1064 as a regulatory PTM that redirects the complex to c-Myc pathway genes and drives breast cancer metastasis, introducing a methyl-mark layer of BAF targeting control.

    Evidence CARM1 KO by zinc-finger nuclease, MS substrate identification, ChIP-seq and migration/metastasis assays

    PMID:24434208

    Open questions at the time
    • Reader of the R1064 methyl mark not yet identified
    • Mechanism redirecting genomic occupancy unresolved
  9. 2014 Medium

    A hypomorphic Baf155 allele produced penetrant exencephaly with proliferation/apoptosis defects, confirming a developmental requirement in neural tube closure beyond complete null lethality.

    Evidence ENU mutagenesis, homozygous mouse model, RNA-seq and proliferation/apoptosis assays

    PMID:24170322

    Open questions at the time
    • Variable transcriptional changes left causal target genes ambiguous
    • Link between specific allele and biochemical defect unclear
  10. 2017 High

    Solved the crystal structure of the SMARCC1 SWIRM/SMARCB1 RPT1 interface, providing atomic detail for core BAF assembly and showing this SWIRM domain is functionally distinct from methyl-lysine-binding SWIRMs.

    Evidence X-ray crystallography with mutagenesis, ITC and NMR titration

    PMID:28438634

    Open questions at the time
    • Did not resolve full assembled complex
    • Functional consequence of disrupting this interface in vivo not tested
  11. 2019 Medium

    Revealed mRNA-level control of SMARCC1 via RBM15/METTL3 m6A methylation and its consequences for radial glia delamination, adding post-transcriptional regulation to SMARCC1 dosage control.

    Evidence RIP, m6A methylation assay, in vivo conditional ablation and transcriptional reporter

    PMID:31020615

    Open questions at the time
    • Site of m6A modification on BAF155 mRNA not mapped
    • Single-lab mechanism
  12. 2021 High

    Refined the oncogenic mechanism of me-BAF155 by showing it recruits BRD4 to super-enhancers and represses interferon pathway genes to evade immunity, and that CARM1 inhibition reverses both, converting a PTM finding into a therapeutic rationale.

    Evidence ChIP-seq, RNA-seq, CARM1 inhibitor, BRD4 co-occupancy and in vivo tumor/metastasis models

    PMID:34865122

    Open questions at the time
    • Direct physical mechanism of BRD4 recruitment by me-BAF155 not resolved
    • Interferon repression mechanism details incomplete
  13. 2021 High

    NMR structures of the SMARCC1 N-terminal MarR-chromo-BRCT module revealed an interconnected fold with a chromodomain that has lost methyl-lysine binding but creates a druggable pocket, defining new structural and therapeutic features.

    Evidence NMR structure determination with cancer-associated missense mutation analysis

    PMID:33953332

    Open questions at the time
    • Functional role of the N-terminal module within the assembled complex unknown
    • Drug-binding pocket not yet pharmacologically exploited
  14. 2021 Medium

    Independent loss-of-function studies established SMARCC1 as a suppressor of PI3K/AKT-driven proliferation and EMT in prostate cancer, broadening its tumor-suppressor role to growth-factor signaling.

    Evidence siRNA knockdown, pathway western blots, cell cycle analysis and xenograft metastasis model

    PMID:34249931

    Open questions at the time
    • Whether suppression is direct transcriptional control of pathway genes unknown
    • Single-lab functional study
  15. 2022 Medium

    Defined the nuclear import machinery for SMARCC1 (KPNA2, Nup50, Nup153), explaining how this nuclear remodeler reaches chromatin.

    Evidence Co-IP, immunofluorescence, importin knockdown and subcellular fractionation

    PMID:35669562

    Open questions at the time
    • NLS within SMARCC1 not mapped
    • Whether import is regulated by signaling unknown
  16. 2023 High

    Genome-scale conditional knockouts showed SMARCC1 establishes accessible chromatin at lineage-specific enhancers in hematopoietic progenitors, cortical neurogenesis, skeletal muscle (via HIF-1α/pSTAT3), and limb enhancers, defining its enhancer-priming function across tissues including a notable GLI-independent role.

    Evidence Conditional KO with ATAC-seq, ChIP-seq, RNA-seq, single-nucleus multiomics and metabolic/transplantation phenotyping

    PMID:37478146 PMID:37805104 PMID:39088321

    Open questions at the time
    • How SMARCC1 selects specific enhancers across tissues unresolved
    • Relationship between enhancer accessibility and downstream TF recruitment incomplete
  17. 2023 High

    RNF138 was identified as the nuclear E3 ligase that K48-polyubiquitinates SMARCC1 at Lys643 to tune inflammatory gene transcription kinetics, pinpointing a site-specific degradation switch controlling SWI/SNF activity at inflammatory loci.

    Evidence Co-IP, K48-specific ubiquitination assay, Lys643 mutagenesis, ChIP and functional genetic screen

    PMID:36800290

    Open questions at the time
    • Signals activating RNF138 toward SMARCC1 not defined
    • Interplay with Wwp2-mediated degradation unclear
  18. 2023 High

    Cross-species rescue established SMARCC1 as causative in human hydrocephalus, with patient variants in SWIRM, Myb-DNA-binding, Glu-rich, and chromo domains failing to rescue Xenopus phenotypes and converging on altered neurogenesis transcription factor expression.

    Evidence Xenopus knockdown, WT vs. patient-variant rescue, OCT imaging and human fetal brain RNA-seq

    PMID:38128548

    Open questions at the time
    • Domain-specific biochemical defects of each variant not dissected
    • Mechanism linking SMARCC1 loss to aqueductal stenosis incomplete
  19. 2025 Medium

    Recent studies extended SMARCC1's regulatory partnerships to PRMT1 (enzyme-independent SWI/SNF recruitment driving chemoresistance), JUND co-regulation of TIMP1 in inflammation, FLOT1-mediated macrophage polarization, and oligodendrocyte differentiation, broadening its transcription-factor and disease repertoire.

    Evidence Co-IP, conditional KO, ChIP/ChIP-qPCR, organoid and xenograft models, and behavioral/myelination phenotyping

    PMID:40108025 PMID:40270464 PMID:40399563 PMID:41423560

    Open questions at the time
    • Whether these TF collaborations share a common recruitment mechanism unknown
    • Direct vs. indirect transcriptional effects not always separated
  20. 2025 Medium

    A preprint linked R1064 methylation to co-transcriptional RNA processing, showing me-BAF155 binds SCAF4/RFX5 and splicing factors and that loss of the mark reduces sense and antisense nascent transcripts without altering chromatin accessibility, implicating SMARCC1 in transcription elongation beyond remodeling.

    Evidence Dimethyl-specific IP-MS, CUT&RUN, TT-seq and R1064K mutant cells (preprint)

    PMID:42239058

    Open questions at the time
    • Not yet peer-reviewed
    • Mechanistic link between me-BAF155 and elongation machinery unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unknown how SMARCC1's many regulatory inputs (R1064 methylation, Lys643 ubiquitination, m6A, importin-mediated localization) are integrated to direct context-specific BAF targeting and to read out into the distinct developmental, metabolic, immune, and tumor-suppressive programs it controls.
  • No unified model linking PTM state to genomic targeting
  • Reader proteins for SMARCC1 modifications largely unidentified
  • Tissue-specific enhancer selection mechanism unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 5 GO:0003677 DNA binding 3 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0042393 histone binding 1
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 2
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-4839726 Chromatin organization 4 R-HSA-74160 Gene expression (Transcription) 4 R-HSA-5357801 Programmed Cell Death 2
Partners
CARM1KPNA2RNF138SMARCA4SMARCB1SMARCD1SMARCE1WWP2
Complex memberships
SWI/SNF (BAF) chromatin remodeling complex

Evidence

Reading pass · 44 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 SRG3 (mouse SMARCC1/BAF155) associates with a mouse SWI2 homolog (BRG1) as detected by co-immunoprecipitation, establishing it as a component of the mammalian SWI/SNF complex. Antisense-mediated reduction of SRG3 protein decreased glucocorticoid-induced apoptosis in the S49.1 thymoma cell line, demonstrating SRG3 is required for glucocorticoid-induced apoptosis. Co-immunoprecipitation; antisense RNA knockdown with apoptosis assay The Journal of experimental medicine Medium 9151708
1999 BAF155 and BRG1 (mammalian SWI/SNF subunits) physically associate with cyclin E and are phosphorylated by cyclin E-associated kinase activity. Overexpression of BRG1 causes growth arrest and senescence-associated beta-galactosidase induction, which is overcome by cyclin E co-expression, indicating cyclin E modulates SWI/SNF chromatin remodeling activity. Co-immunoprecipitation; overexpression with growth arrest and senescence assays; in vitro kinase assay Molecular and cellular biology Medium 9891079
2001 Homozygous Srg3 null mice undergo rapid degeneration after early implantation; inner cell mass degenerates in vitro after blastocyst culture, establishing Srg3 as essential for early embryogenesis. Approximately 20% of heterozygous embryos develop exencephaly due to failure of neural fold elevation, indicating a role in brain development. Gene knockout (null mutation); in vitro blastocyst outgrowth; histological analysis Molecular and cellular biology High 11604513
2001 SRG3 associates with the glucocorticoid receptor (GR) in the thymus. Transgenic overexpression of SRG3 in peripheral T cells induces formation of the SRG3-GR complex and renders peripheral T cells sensitive to glucocorticoid-induced apoptosis. A dominant-negative SRG3 mutant that blocks the SRG3-GR complex decreases GC sensitivity in thymoma cells. Co-immunoprecipitation; transgenic overexpression; dominant-negative mutant; apoptosis assay Journal of immunology High 11441086
2001 Activated Notch1 (NotchIC) downregulates SRG3 promoter activity and SRG3 expression in thymocytes, conferring resistance to glucocorticoid-induced apoptosis. Transgenic SRG3 overexpression restores GC sensitivity in Notch1-transgenic thymocytes, placing SRG3 downstream of Notch1 in regulating GC sensitivity. Promoter activity assay; transgenic mouse rescue experiment; apoptosis assay Proceedings of the National Academy of Sciences of the United States of America Medium 11504912
2004 TCR signaling represses SRG3 gene expression via Ras/MEK/ERK and PI3K pathways, acting through E protein and Ets transcription factor binding sites in the SRG3 promoter, thereby rendering primary thymocytes resistant to glucocorticoid-induced apoptosis. Mutation of these promoter elements abolishes TCR/Ras-mediated repression. Pharmacological inhibitors; promoter mutagenesis; reporter assay; apoptosis assay The Journal of biological chemistry Medium 15016814
2004 E2A/HEB heterodimers bind to an E-box element in the SRG3 promoter to activate SRG3 transcription. Id3, induced by TCR signaling via MEK/ERK, inhibits E2A/HEB binding to the E-box and represses SRG3 expression, thereby conferring glucocorticoid resistance. Overexpression of SRG3 overcomes Id3-mediated GC resistance. Promoter reporter assay; chromatin immunoprecipitation; retroviral transduction; apoptosis rescue assay The Journal of biological chemistry Medium 15016815
2004 Nitric oxide (NO) represses SRG3 transcription by inactivating the transcription factor Sp1's DNA-binding activity at the SRG3 promoter. Overexpression of SRG3 from a heterologous promoter reduces NO-mediated rescue of thymocytes from GC-induced apoptosis, placing SRG3 downstream of NO in the regulation of GC sensitivity. Promoter reporter assay; EMSA; SRG3 overexpression; apoptosis assay The Journal of biological chemistry Medium 15187086
2005 BAF155 and BAF170 protein levels limit the maximum cellular amount of BAF57 through protein-protein interactions that protect BAF57 from proteasomal degradation. Domains mediating BAF155-BAF57 interaction were mapped by deletion mutagenesis, and disruption of these interactions increases proteasomal degradation of BAF57. Co-immunoprecipitation; deletion mutagenesis; proteasome inhibitor assay; western blot Molecular and cellular biology Medium 16199878
2005 SRG3 enhances androgen receptor (AR) transactivation in prostate cells through multiple mechanisms: (1) SRG3 is induced by androgen via AR, forming a positive feedback loop; (2) SRG3 upregulates the coactivator SRC-1 protein level; (3) the AR/SRG3/SRC-1 complex functions independently of BRG1/BRM, as demonstrated in BRG1/BRM-deficient C33A cells. ChIP shows the AR/SRG3/SRC-1 complex occupies androgen response elements on the SRG3 and PSA promoters in an androgen-dependent manner. Reporter assay; western blot; chromatin immunoprecipitation; BRG1/BRM-deficient cell assay Molecular and cellular biology High 15923603
2005 SRG3 gene expression is regulated by cooperative interactions between Sp1/Sp3 and Ets transcription factors binding to GC boxes and Ets sites in the proximal SRG3 promoter. Sp-mediated activation requires intact Ets-binding elements, with combinatorial Sp/Ets factor expression yielding synergistic activation or repression. Reporter assay; EMSA; Drosophila SL2 cell transfection system; promoter mutagenesis Biochemical and biophysical research communications Medium 16288722
2005 Deltex1 (a Notch1 effector) competitively inhibits p300 binding to E2A/HEB at E-box elements on the SRG3 promoter, thereby repressing SRG3 transcription and conferring glucocorticoid resistance in double-positive thymocytes. RBP-J represses SRG3 transcription through N-box elements. Promoter reporter assay; competitive binding assay; transgenic rescue; apoptosis assay Cell death and differentiation Medium 16341126
2007 SRG3 directly interacts with SNF5 (via SWIRM domain), BRG1 (via SANT domain), and BAF60a. SRG3 stabilizes these SWI/SNF components by attenuating their proteasomal degradation, as validated in SRG3 transgenic and haploinsufficient mouse cells. Co-immunoprecipitation; domain deletion mutagenesis; proteasome inhibitor assay; transgenic and knockout mouse cells The Journal of biological chemistry High 17255092
2007 Srg3-deficient embryos rescued by transgenic expression lack SRG3 in visceral endoderm of yolk sac, leading to defective blood vessel formation and reduced expression of angiogenesis-related genes (Angiopoietin1, Tie2, EphrinB2, Ihh, Notch1), establishing SRG3 as required for angiogenesis and visceral endoderm development. Conditional transgenic rescue; in situ hybridization; gene expression analysis; histology Developmental biology Medium 18206867
2009 Smarcc1/Baf155 knockdown in mouse ESCs suppresses repression of Nanog and other self-renewal genes upon differentiation, independently of Oct4. Mechanistic studies show Smarcc1 expression is necessary for heterochromatin formation and chromatin compaction during differentiation, coupling gene repression with chromatin structural changes. RNAi knockdown; functional genetic screen; chromatin compaction assay; Nanog reporter Stem cells (Dayton, Ohio) Medium 19785031
2010 Srg3 deficiency promotes G1 cell cycle arrest and antagonizes apoptotic response to DNA damage by robustly inducing p53 and p21 proteins. DNA damage signals promote Srg3 degradation in a p53-dependent manner, and Srg3 heterozygous mice are prone to sarcoma formation enhanced by p53 haploinsufficiency, placing Srg3 in the p53/p21 tumor suppressor pathway. Knockout/heterozygous mouse model; western blot; cell cycle analysis; tumor incidence study Oncogene High 20935679
2011 Re-expression of full-length but not truncated BAF155 in BAF155-deficient cancer cell lines (SNUC2B, SKOV3) reduces colony formation via replicative senescence but not apoptosis, identifying the C-terminal proline-glutamine rich domain as critical for tumor suppressor activity. Re-expression of wild-type and truncated BAF155 in null cell lines; colony formation assay; senescence assay Epigenetics Medium 22139574
2012 CHFR E3 ubiquitin ligase interacts with and ubiquitinates BRG1, SNF5, and BAF60a to target them for proteasomal degradation. SRG3/mBAF155 stabilizes these components by blocking their interaction with CHFR, thus protecting them from CHFR-mediated ubiquitination. Co-immunoprecipitation; ubiquitination assay; proteasome inhibitor assay Biochemical and biophysical research communications Medium 22285184
2013 Wwp2 E3 ubiquitin ligase interacts with SRG3 (SMARCC1) via WW domain-PPPY motif interaction, co-localizes with SRG3 in the nucleus, and promotes SRG3 ubiquitination and proteasomal degradation. A catalytically inactive Wwp2 mutant abolishes SRG3 ubiquitination. Co-immunoprecipitation; ubiquitination assay; catalytic-dead mutant; proteasome inhibitor assay Biochemical and biophysical research communications Medium 24365151
2014 CARM1 methylates BAF155 at arginine R1064. This methylation directs methylated BAF155 to unique chromatin regions including c-Myc pathway genes, regulates breast cancer cell migration and metastasis, and is identified as an independent prognostic biomarker. CARM1 knockout was achieved using Zinc-Finger Nuclease technology. CARM1 KO by Zinc-Finger Nuclease; mass spectrometry substrate identification; ChIP-seq; migration/metastasis assays Cancer cell High 24434208
2014 A missense allele of Baf155 (Baf155mps3) causes highly penetrant exencephaly in homozygous mice, with defects in proliferation and apoptosis within the neural tube. RNA-Seq reveals few but variable gene expression changes, suggesting inconsistent gene regulation contributes to failed neural tube closure. ENU mutagenesis; homozygous mouse model; RNA-Seq; proliferation/apoptosis assays Developmental neurobiology Medium 24170322
2017 The SWIRM domain of BAF155 is responsible for its interaction with BAF47 (SMARCB1), specifically via the Repeat 1 (RPT1) domain of BAF47. Crystal structure of the SWIRM/RPT1 complex was solved at high resolution; mutagenesis, ITC, and NMR titrations validated the interaction interface. The BAF155 SWIRM domain is functionally distinct from other SWIRM domains that bind methylated lysines. Crystal structure determination; mutagenesis; isothermal titration calorimetry; NMR titration Journal of molecular biology High 28438634
2018 Conditional deletion of BAF155 in the developing cortex diminishes basal intermediate progenitor (bIP) pool and increases basal radial glia (bRG) due to apical RG delamination. BAF155 is required for normal PAX6 transcription factor activity and regulates PAX6-dependent expression of the CDC42 effector protein CEP4 to control progenitor delamination. Conditional knockout; immunofluorescence; gene expression analysis; rescue experiments iScience Medium 30240734
2019 RBM15 interacts with BAF155 mRNA and mediates its degradation through the m6A mRNA methylation machinery (requiring METTL3). RBM15 ablation augments BAF155 expression; RBM15 overexpression decreases BAF155 mRNA and protein and perturbs BAF155-dependent transcriptional activity and apical radial glia delamination in vivo. RIP; m6A methylation assay; in vivo conditional ablation; overexpression; transcriptional reporter Molecular neurobiology Medium 31020615
2019 BAF155 directly interacts with HBx (Hepatitis B virus X protein) via its SANT domain binding to HBx residues 81–120. BAF155 competes with the 20S proteasome subunit PSMA7 to bind HBx, protecting HBx from ubiquitin-independent proteasomal degradation and enhancing HBx transcriptional transactivation function. Co-immunoprecipitation; siRNA knockdown; domain mapping; proteasome competition assay; transcriptional assay Emerging microbes & infections Medium 31533543
2020 Crystal structure and NMR analysis of the hSNF5 RPT1 domain/BAF155 SWIRM complex reveals that the N-terminal region of hSNF5 undergoes a coil-to-helix transition upon binding, forming a new αN helix that interacts with the β2-α1 loop of hSNF5 via hydrogen bonds and with BAF155 SWIRM via hydrophobic contacts. Multi-angle light scattering confirmed a 1:1 heterodimeric complex. X-ray crystallography; NMR spectroscopy; multi-angle light scattering; biophysical binding assays International journal of molecular sciences High 32244797
2021 Methylated BAF155 (me-BAF155 at R1064) promotes tumor metastasis via two mechanisms: (1) activation of super-enhancer-addicted oncogenes by recruiting BRD4, and (2) repression of interferon α/γ pathway genes to suppress host immune response. Pharmacological CARM1 inhibition abrogates oncogene expression and boosts cytotoxic T cell activity and tumor infiltration. ChIP-seq; RNA-seq; CARM1 inhibitor treatment; in vitro migration assay; in vivo tumor/metastasis model; BRD4 co-occupancy analysis Nucleic acids research High 34865122
2021 Structural analysis revealed the N-terminus of BAF155/SMARCC1 contains a MarR-like domain, a chromodomain, and a BRCT domain that form an interconnected module. In this structure the chromodomain makes interdomain contacts and has lost its canonical function to bind methylated lysines. Two adjacent conserved pockets in the cleft between domains form a potential drug-binding site targetable by small molecules. NMR structure determination; domain boundary mapping; functional validation of cancer-associated missense mutations Communications biology High 33953332
2021 SMARCC1 loss in prostate cancer cells activates the PI3K/AKT signaling pathway, promoting cell proliferation by advancing cell cycle and inducing EMT-mediated migration. SMARCC1 depletion facilitates xenograft tumor growth and lung metastasis in mice, establishing SMARCC1 as a suppressor of the PI3K/AKT pathway. siRNA knockdown; western blot for PI3K/AKT pathway; cell cycle analysis; xenograft mouse model Frontiers in cell and developmental biology Medium 34249931
2022 SMARCC1 is transported into the nucleus via interaction with the importin KPNA2, as well as nuclear pore components Nup50 and Nup153. Knockdown of KPNA2, Nup50, or Nup153 reduces nuclear SMARCC1 while increasing cytoplasmic SMARCC1, establishing KPNA2-dependent nuclear import as the mechanism for SMARCC1 nuclear localization. Co-immunoprecipitation; immunofluorescence; siRNA knockdown of importins; subcellular fractionation Frontiers in molecular biosciences Medium 35669562
2022 SMARCC1 and BAF57 (SMARCE1) interaction was characterized; the assembly mechanism of BAF core subunits was studied by co-expressing binary, ternary and tetrameric complexes. The minimal SMARCC1 fragment (residues 862–966) and SMARCE1 fragment (residues 210–284) form crystals with diffraction data to 3.2 Å, defining the interacting amino acid regions. Recombinant co-expression; crystallography; crystal diffraction Biochemical and biophysical research communications Medium 35158202
2023 RNF138, a nuclear E3 ubiquitin ligase, interacts with SMARCC1 and mediates K48-linked polyubiquitination of SMARCC1 at position Lys643, targeting it for proteasomal degradation. This fine-tunes late inflammatory gene transcription kinetics by inhibiting SWI/SNF-mediated chromatin remodeling at inflammatory gene loci. Co-immunoprecipitation; ubiquitination assay with K48-linkage specificity; site-specific mutagenesis (Lys643); ChIP; functional genetic screen Cell reports High 36800290
2023 Irf7 transcriptionally activates Srg3 (SMARCC1) expression. Srg3 in turn promotes NF-κB signaling pathway activation and ferroptosis in lung cells, and promotes M1 macrophage polarization, exacerbating septic lung injury. Specific inhibition of Irf7 or Srg3 knockdown improves ALI symptoms. AAV9-mediated in vivo Srg3 knockdown; LPS-induced cell model; KEGG pathway analysis; gain/loss-of-function experiments; Irf7 ChIP/reporter Cellular & molecular biology letters Medium 37946128
2023 Smarcc1 knockdown in Xenopus tropicalis recapitulates aqueductal stenosis and cardiac defects seen in human hydrocephalus patients. Wild-type human SMARCC1 rescues these phenotypes but patient-specific SMARCC1 variants (localizing to SWIRM, Myb-DNA binding, Glu-rich, and Chromo domains) do not. Mutant human fetal brain and Smarcc1-mutant Xenopus brain show similar altered expression of neurogenesis transcription factors NEUROD2 and MAB21L2. Xenopus Smarcc1 knockdown; in vivo rescue with WT vs. patient-variant SMARCC1; OCT imaging; RNA-seq of human fetal brain Brain : a journal of neurology High 38128548
2023 SMARCC1 maintains chromatin accessibility at active limb enhancers including those bound by GLI transcription factors, but does not mediate GLI3-dependent transcriptional repression. SMARCC1 binding at GLI-regulated enhancers occurs independently of GLI3. Most GLI target genes are unaffected in Smarcc1 conditional knockouts, and SMARCC1 is not required for constitutive GLI repression in HH mutant limb buds. Conditional knockout; ATAC-seq; ChIP-seq; RNA-seq; GLI3 mutant epistasis Developmental biology High 37805104
2024 IRF1 regulates SMARCC1 expression by recruiting histone modifiers GCN5 (H3K27ac writer) and SETD2 (H3K4me3 writer) to the SMARCC1 promoter and 10 kb upstream region. Overexpression of GCN5 or SETD2 restores SMARCC1 expression and exacerbates OA-like symptoms. Knockdown of IRF1 or SMARCC1 mitigates OA-like symptoms and reduces M1 macrophage polarization. ChIP for histone marks; GCN5/SETD2 overexpression rescue; siRNA knockdown in vivo and in vitro; OA rat model Journal of orthopaedic translation Medium 38586591
2024 Baf155-deficient hematopoietic stem and progenitor cells (HSPCs) fail to establish accessible chromatin at putative enhancers containing binding motifs for hematopoietic lineage transcription factors, resulting in reduced mature blood cell output, particularly neutrophils, B cells, and CD8+ T cells, and failure of hematopoietic regeneration upon transplantation. Conditional knockout; single-nucleus multiomics (ATAC-seq + RNA-seq); transplantation assay; 5-FU injury model Cell reports High 39088321
2023 Baf155 modulates the DNA-binding activity of HIF-1α to promoters of its target genes in skeletal muscle. Baf155 requires phospho-STAT3 (pSTAT3), which forms a coactivator complex with HIF-1α, to activate HIF-1α signaling. Muscle-specific ablation of Baf155 increases oxidative metabolism, decreases lactate production, raises intramuscular ATP, and enhances endurance exercise capacity. Muscle-specific conditional knockout; ChIP for HIF-1α binding; metabolic assays; exercise capacity testing PLoS biology High 37478146
2025 PRMT1 recruits the SWI/SNF complex via direct interaction with SMARCC1, leading to transcriptional activation of IGF2BP2 and carboplatin resistance in head and neck squamous cell carcinoma. This function is independent of PRMT1's enzymatic (methyltransferase) activity. Co-immunoprecipitation; conditional PRMT1 KO; ChIP; patient-derived organoids; xenograft model; catalytic-dead mutant Advanced science Medium 40270464
2025 SMARCC1 activates FLOT1 transcription by binding to its promoter (demonstrated by ChIP), thereby promoting M2 macrophage polarization and reducing ferroptosis (maintaining GSH:GSSG ratio and reducing lipid peroxidation). SMARCC1 knockdown reduces M2 macrophage migration and polarization, and these effects are rescued by FLOT1 overexpression. ChIP; siRNA knockdown; co-culture assay; ferroptosis assay (GSH:GSSG, lipid peroxidation, TEM); xenograft model Journal of molecular medicine Medium 40108025
2025 BAF155 methylation at R1064 (deposited by CARM1/PRMT4) selectively enhances BAF155 interactions with RNA processing factors including SCAF4, splicing factors, and RFX5, demonstrated by immunoprecipitation-mass spectrometry with a dimethyl-specific antibody. CUT&RUN shows BAF155me2a co-occupies promoters with SCAF4 and RFX5. Loss of R1064 methylation (R1064K mutant) reduces 5' sense transcripts and upstream antisense transcripts (PROMPTs) at BAF155-bound promoters without altering chromatin accessibility or BAF155 genomic occupancy, implicating a co-transcriptional role in RNA elongation. Immunoprecipitation-mass spectrometry (dimethyl-specific antibody); CUT&RUN; TT-seq (nascent transcription); methylation-deficient R1064K mutant cells bioRxivpreprint Medium 42239058
2024 Reduced CARM1 activity and upregulation of BAF155 at the 4-cell stage promote early cell polarization and trophectoderm (TE) specification in mouse embryos, linking CARM1-mediated arginine methylation of BAF155 to the first lineage allocation decision. Live imaging; CARM1 activity perturbation; BAF155 overexpression; lineage tracing in mouse embryos bioRxivpreprint Low bio_10.1101_2024.07.26.605266
2025 BAF155 is highly expressed in committed oligodendrocyte precursor cells (OPCs) and regulates OPC differentiation and myelination by coordinating expression of synapse-related genes mediating OPC-neuron synaptic communication. BAF155-dependent chromatin regulation varies across brain regions, contributing to local myelin deficits and ASD-like behavioral phenotypes in mice. Conditional knockout; RNA-seq; chromatin assays; behavioral testing Nature communications Medium 41423560
2025 SMARCC1 collaborates with the transcription factor JUND to co-regulate TIMP1 expression in COVID-19 monocytes. The inflammatory metabolite 7α,25-OHC enhances SMARCC1-JUND interactions and promotes SMARCC1 co-localization with H3K27ac marks at the TIMP1 promoter, activating TIMP1 transcription. Co-immunoprecipitation; ChIP-qPCR; scRNA-seq/ATAC-seq analysis; 7α,25-OHC treatment Cellular and molecular life sciences Medium 40399563

Source papers

Stage 0 corpus · 64 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 CARM1 methylates chromatin remodeling factor BAF155 to enhance tumor progression and metastasis. Cancer cell 203 24434208
2001 Srg3, a mouse homolog of yeast SWI3, is essential for early embryogenesis and involved in brain development. Molecular and cellular biology 168 11604513
1999 Cyclin E associates with BAF155 and BRG1, components of the mammalian SWI-SNF complex, and alters the ability of BRG1 to induce growth arrest. Molecular and cellular biology 140 9891079
2009 Smarcc1/Baf155 couples self-renewal gene repression with changes in chromatin structure in mouse embryonic stem cells. Stem cells (Dayton, Ohio) 125 19785031
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
2013 miR-320c regulates gemcitabine-resistance in pancreatic cancer via SMARCC1. British journal of cancer 99 23799850
2009 Dysregulation of the transcription factors SOX4, CBFB and SMARCC1 correlates with outcome of colorectal cancer. British journal of cancer 96 19156145
2007 SRG3 interacts directly with the major components of the SWI/SNF chromatin remodeling complex and protects them from proteasomal degradation. The Journal of biological chemistry 79 17255092
2021 BAF155 methylation drives metastasis by hijacking super-enhancers and subverting anti-tumor immunity. Nucleic acids research 51 34865122
2023 Irf7 regulates the expression of Srg3 and ferroptosis axis aggravated sepsis-induced acute lung injury. Cellular & molecular biology letters 49 37946128
2019 RBM15 Modulates the Function of Chromatin Remodeling Factor BAF155 Through RNA Methylation in Developing Cortex. Molecular neurobiology 49 31020615
2011 Identification of a core member of the SWI/SNF complex, BAF155/SMARCC1, as a human tumor suppressor gene. Epigenetics 47 22139574
1997 A new mouse gene, SRG3, related to the SWI3 of Saccharomyces cerevisiae, is required for apoptosis induced by glucocorticoids in a thymoma cell line. The Journal of experimental medicine 41 9151708
2008 SMARCC1 expression is upregulated in prostate cancer and positively correlated with tumour recurrence and dedifferentiation. Histology and histopathology 37 18581278
2007 SRG3, a core component of mouse SWI/SNF complex, is essential for extra-embryonic vascular development. Developmental biology 34 18206867
2018 MicroRNA-202-5p functions as a tumor suppressor in colorectal carcinoma by directly targeting SMARCC1. Gene 32 30144500
2014 A unique missense allele of BAF155, a core BAF chromatin remodeling complex protein, causes neural tube closure defects in mice. Developmental neurobiology 32 24170322
2018 Chromatin Remodeling BAF155 Subunit Regulates the Genesis of Basal Progenitors in Developing Cortex. iScience 30 30240734
2017 Structural Insights into BAF47 and BAF155 Complex Formation. Journal of molecular biology 29 28438634
2001 Peripheral T cells become sensitive to glucocorticoid- and stress-induced apoptosis in transgenic mice overexpressing SRG3. Journal of immunology (Baltimore, Md. : 1950) 29 11441086
2001 Notch1 confers a resistance to glucocorticoid-induced apoptosis on developing thymocytes by down-regulating SRG3 expression. Proceedings of the National Academy of Sciences of the United States of America 27 11504912
2005 Modulation of androgen receptor transactivation by the SWI3-related gene product (SRG3) in multiple ways. Molecular and cellular biology 26 15923603
2020 CircRNA SMARCC1 Sponges MiR-140-3p to Regulate Cell Progression in Colorectal Cancer. Cancer management and research 23 32606978
2023 RNF138 inhibits late inflammatory gene transcription through degradation of SMARCC1 of the SWI/SNF complex. Cell reports 21 36800290
2004 E2A/HEB and Id3 proteins control the sensitivity to glucocorticoid-induced apoptosis in thymocytes by regulating the SRG3 expression. The Journal of biological chemistry 19 15016815
2004 T cell receptor signaling inhibits glucocorticoid-induced apoptosis by repressing the SRG3 expression via Ras activation. The Journal of biological chemistry 18 15016814
2005 Notch1 confers thymocytes a resistance to GC-induced apoptosis through Deltex1 by blocking the recruitment of p300 to the SRG3 promoter. Cell death and differentiation 17 16341126
2022 Capecitabine Regulates HSP90AB1 Expression and Induces Apoptosis via Akt/SMARCC1/AP-1/ROS Axis in T Cells. Oxidative medicine and cellular longevity 16 35368874
2024 A novel SMARCC1 BAFopathy implicates neural progenitor epigenetic dysregulation in human hydrocephalus. Brain : a journal of neurology 15 38128548
2021 SMARCC1 Suppresses Tumor Progression by Inhibiting the PI3K/AKT Signaling Pathway in Prostate Cancer. Frontiers in cell and developmental biology 15 34249931
2010 Srg3, a mouse homolog of BAF155, is a novel p53 target and acts as a tumor suppressor by modulating p21(WAF1/CIP1) expression. Oncogene 15 20935679
2019 Chromatin remodelling factor BAF155 protects hepatitis B virus X protein (HBx) from ubiquitin-independent proteasomal degradation. Emerging microbes & infections 14 31533543
2007 Expression of SRG3, a chromatin-remodelling factor, in the mouse oocyte and early preimplantation embryos. Zygote (Cambridge, England) 14 17462105
2021 Chromatin Regulator SRG3 Overexpression Protects against LPS/D-GalN-Induced Sepsis by Increasing IL10-Producing Macrophages and Decreasing IFNγ-Producing NK Cells in the Liver. International journal of molecular sciences 13 33809795
2018 A mendelian form of neural tube defect caused by a de novo null variant in SMARCC1 in an identical twin. Annals of neurology 13 29360170
2023 Baf155 regulates skeletal muscle metabolism via HIF-1a signaling. PLoS biology 12 37478146
2022 SMARCC1 Enters the Nucleus via KPNA2 and Plays an Oncogenic Role in Bladder Cancer. Frontiers in molecular biosciences 11 35669562
2021 Ubiquitous Overexpression of Chromatin Remodeling Factor SRG3 Exacerbates Atopic Dermatitis in NC/Nga Mice by Enhancing Th2 Immune Responses. International journal of molecular sciences 11 33557054
2012 SRG3/mBAF155 stabilizes the SWI/SNF-like BAF complex by blocking CHFR mediated ubiquitination and degradation of its major components. Biochemical and biophysical research communications 11 22285184
2015 Ubiquitous Over-Expression of Chromatin Remodeling Factor SRG3 Ameliorates the T Cell-Mediated Exacerbation of EAE by Modulating the Phenotypes of both Dendritic Cells and Macrophages. PloS one 10 26147219
2010 Smarcc1 expression: a significant predictor of disease-specific survival in patients with clinically localized prostate cancer treated with no intention to cure. Scandinavian journal of urology and nephrology 10 21087120
2021 SWI/SNF subunit BAF155 N-terminus structure informs the impact of cancer-associated mutations and reveals a potential drug binding site. Communications biology 9 33953332
2013 Wwp2 targets SRG3, a scaffold protein of the SWI/SNF-like BAF complex, for ubiquitination and degradation. Biochemical and biophysical research communications 9 24365151
2005 Expression of SRG3, a core component of mouse SWI/SNF chromatin-remodeling complex, is regulated by cooperative interactions between Sp1/Sp3 and Ets transcription factors. Biochemical and biophysical research communications 7 16288722
2004 Nitric oxide inhibits glucocorticoid-induced apoptosis of thymocytes by repressing the SRG3 expression. The Journal of biological chemistry 7 15187086
2025 SMARCC1 promotes M2 macrophage polarization and reduces ferroptosis in lung cancer by activating FLOT1 transcription. Journal of molecular medicine (Berlin, Germany) 5 40108025
2025 PRMT1-Mediated SWI/SNF Complex Recruitment via SMARCC1 Drives IGF2BP2 Transcription to Enhance Carboplatin Resistance in Head and Neck Squamous Cell Carcinoma. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 5 40270464
2024 IRF1 governs the expression of SMARCC1 via the GCN5-SETD2 axis and actively engages in the advancement of osteoarthritis. Journal of orthopaedic translation 5 38586591
2024 Baf155 controls hematopoietic differentiation and regeneration through chromatin priming. Cell reports 5 39088321
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
2005 Monoclonal antibodies reactive with the BAF155 (SMARCC1) and BAF170 (SMARCC2) components of human SWI/SNF-related complexes. Hybridoma (2005) 4 15785210
2023 First reports of fetal SMARCC1 related hydrocephalus. European journal of medical genetics 3 37285932
2023 SMARCC1 is a susceptibility gene for congenital hydrocephalus with an autosomal dominant inheritance mode and incomplete penetrance. Prenatal diagnosis 3 37639281
2020 A Coil-to-Helix Transition Serves as a Binding Motif for hSNF5 and BAF155 Interaction. International journal of molecular sciences 3 32244797
2024 Overexpression of Chromatin Remodeling Factor SRG3 Down-Regulates IL1β-Expressing M1 Macrophages and IL17-Producing T Cells in Adipose Tissues. International journal of molecular sciences 2 39519233
2014 CARM1 and BAF155: an example of how chromatin remodeling factors can be relocalized and contribute to cancer. Breast cancer research : BCR 1 25927994
2026 Arginine methylation of BAF155 regulates interactions with RNA processing machinery. bioRxiv : the preprint server for biology 0 42239058
2025 Inflammatory metabolite 7α,25-OHC promotes TIMP1 expression in COVID-19 monocytes through synergy effect of SMARCC1/JUND/H3K27ac. Cellular and molecular life sciences : CMLS 0 40399563
2025 Chromatin remodeling factor BAF155 coordinates oligodendroglial-neuronal communications linked to regional myelination and autism-like behavioral deficits in mice. Nature communications 0 41423560
2023 The BAF chromatin complex component SMARCC1 does not mediate GLI transcriptional repression of Hedgehog target genes in limb buds. bioRxiv : the preprint server for biology 0 36798239
2023 A novel SMARCC1 -mutant BAFopathy implicates epigenetic dysregulation of neural progenitors in hydrocephalus. medRxiv : the preprint server for health sciences 0 36993720
2023 The BAF chromatin complex component SMARCC1 does not mediate GLI transcriptional repression of Hedgehog target genes in limb buds. Developmental biology 0 37805104
2013 1H, 15N, and 13C resonance assignments and secondary structure of the SWIRM domain of human BAF155, a chromatin remodeling complex component. Molecules and cells 0 23996527
2010 Normal Adult Hippocampal Neurogenesis in SRG3-overexpressing Transgenic Mice. Experimental neurobiology 0 22110340

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