Affinage

SMARCC1

SWI/SNF complex subunit SMARCC1 · UniProt Q92922

Length
1105 aa
Mass
122.9 kDa
Annotated
2026-04-28
65 papers in source corpus 41 papers cited in narrative 41 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMARCC1 (BAF155/SRG3) is a scaffold subunit of the mammalian SWI/SNF (BAF) chromatin remodeling complex that stabilizes core complex components, integrates diverse transcription factor inputs, and is essential for embryonic development, neural tube closure, hematopoietic lineage priming, and multiple tissue-specific gene regulatory programs. Its SWIRM domain directly binds SNF5/BAF47 through a coil-to-helix transition, its SANT domain contacts BRG1, and its C-terminal region binds BAF57 and BAF60a; SMARCC1 stabilizes these partners by blocking CHFR-mediated ubiquitination and proteasomal degradation, while its own turnover is regulated by RNF138-mediated K48-polyubiquitination at K643 and by RBM15/METTL3-dependent mRNA decay (PMID:17255092, PMID:28438634, PMID:32244797, PMID:22285184, PMID:36800290, PMID:31020615). CARM1-mediated methylation of SMARCC1 at R1064 redirects SWI/SNF to super-enhancers of oncogenes and represses interferon pathway genes, linking post-translational modification of this scaffold to metastatic and immune-evasive transcriptional programs (PMID:24434208, PMID:34865122). Loss-of-function variants in SMARCC1 cause congenital hydrocephalus with aqueductal stenosis and cardiac defects, as demonstrated by patient-specific variant modeling in Xenopus and human fetal brain transcriptomics (PMID:38128548).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1997 Medium

    Identification of SMARCC1/SRG3 as a core SWI/SNF component associated with BRG1 and required for glucocorticoid-induced thymocyte apoptosis established it as a functionally important chromatin remodeling subunit rather than a passive structural element.

    Evidence Immunoprecipitation with BRG1 and antisense knockdown apoptosis assay in thymoma cells

    PMID:9151708

    Open questions at the time
    • Antisense knockdown lacks genetic specificity; direct protein-protein binding not shown
  2. 1998 High

    Reconstitution of direct interactions between the yeast SMARCC1 ortholog (Rsc8) and both the ATPase (Sth1) and BAF60 homolog (Rsc6) defined the conserved structural core of SWI/SNF-family complexes.

    Evidence In vitro binding of bacterially produced proteins plus two-hybrid and genetic suppression in yeast

    PMID:9685490

    Open questions at the time
    • Mammalian orthologs not yet tested in vitro at this stage
  3. 2001 High

    Knockout and transgenic mouse studies demonstrated that SMARCC1 is essential for early embryogenesis (inner cell mass survival), neural tube closure, and glucocorticoid-induced apoptosis via physical association with the glucocorticoid receptor, establishing SMARCC1 as indispensable for both development and hormone-dependent cell death.

    Evidence Homozygous null and heterozygous mouse embryos; transgenic overexpression and dominant-negative mutant in T cells; Co-IP of SRG3–GR complex

    PMID:11441086 PMID:11504912 PMID:11604513

    Open questions at the time
    • Molecular targets of SRG3 in neural fold elevation not identified
    • Whether GR interaction is direct or bridged by other SWI/SNF subunits was unresolved
  4. 2004 High

    Dissection of SRG3 promoter regulation by TCR/Notch1/E-protein/Id3 pathways revealed that SRG3 transcriptional level is the critical rheostat for glucocorticoid sensitivity in thymocytes, integrating multiple signaling inputs onto E-box and Ets elements.

    Evidence Promoter-reporter assays, EMSA, site-directed mutagenesis, pharmacological pathway inhibitors, retroviral epistasis rescue in primary thymocytes

    PMID:15016814 PMID:15016815

    Open questions at the time
    • Chromatin-level regulation (histone marks) at the endogenous SRG3 locus not examined
    • In vivo ChIP confirmation of factor occupancy lacking
  5. 2005 High

    Domain mapping revealed that the SWIRM domain mediates SNF5 binding and the SANT domain mediates BRG1 binding, while SMARCC1 stabilizes these and BAF57 by preventing their proteasomal degradation, establishing SMARCC1 as the stoichiometry-maintaining scaffold of the mammalian SWI/SNF complex.

    Evidence Co-IP with domain deletions, proteasome inhibitor assays, transgenic and haploinsufficient mouse validation

    PMID:16199878 PMID:17255092

    Open questions at the time
    • E3 ligase responsible for partner degradation not yet identified
    • Structural basis of SWIRM–SNF5 interaction unresolved
  6. 2005 High

    Demonstration that SRG3 coactivates androgen receptor transactivation even in BRG1/BRM-deficient cells revealed a SWI/SNF ATPase-independent transcriptional coactivator function, broadening SMARCC1's role beyond canonical chromatin remodeling.

    Evidence Reporter assay, ChIP, Co-IP in BRG1/BRM-null SW13 cells

    PMID:15923603

    Open questions at the time
    • Mechanism of ATPase-independent coactivation not defined
    • Whether this involves SRC-1 stabilization exclusively was uncertain
  7. 2009 High

    Functional genetic screening in mESCs showed that SMARCC1 is required for heterochromatin formation, chromatin compaction, and repression of Nanog during differentiation, linking SMARCC1 to the exit from pluripotency.

    Evidence shRNA screen with Nanog reporter, heterochromatin staining, chromatin compaction assay in mESCs

    PMID:19785031

    Open questions at the time
    • Whether SMARCC1 acts via PBAF specifically versus other BAF assemblies in ESCs remained unclear
    • Direct genomic targets mediating compaction not mapped
  8. 2012 Medium

    Identification of CHFR as the E3 ligase targeting BRG1/SNF5/BAF60a for degradation, with SMARCC1 blocking CHFR access, provided the molecular mechanism underlying SMARCC1's complex-stabilizing role.

    Evidence Co-IP, ubiquitination assay, competition assay, proteasome inhibitor

    PMID:22285184

    Open questions at the time
    • Single-lab finding without independent replication
    • In vivo confirmation of CHFR-SMARCC1 competition not performed
  9. 2014 High

    Discovery that CARM1 methylates SMARCC1 at R1064 and that this modification redirects SWI/SNF occupancy to c-Myc pathway loci established post-translational modification as a mechanism to reprogram SWI/SNF targeting in breast cancer.

    Evidence CARM1 ZFN knockout, mass spectrometry substrate discovery, ChIP-seq, migration assay

    PMID:24434208

    Open questions at the time
    • Whether R1064 methylation alters BAF subunit composition was unknown
    • Reader of the methyl mark not identified
  10. 2017 High

    Crystal structure of the BAF155 SWIRM–BAF47 RPT1 complex revealed that SWIRM serves as a modular protein-protein interaction domain rather than a DNA-binding domain, and a follow-up structure showed BAF47 undergoes a coil-to-helix transition upon binding, with the interface overlapping Rhabdoid tumor mutation sites.

    Evidence X-ray crystallography, ITC, NMR, extensive mutagenesis

    PMID:28438634 PMID:32244797

    Open questions at the time
    • Full-length complex structure not available
    • How Rhabdoid mutations mechanistically disrupt complex assembly in cells not fully resolved
  11. 2021 High

    Methylated BAF155 was shown to promote metastasis through two epigenomic mechanisms—activating super-enhancer-addicted oncogenes via BRD4 recruitment and repressing interferon pathway genes—demonstrating that a single post-translational mark on a scaffold subunit simultaneously drives tumor cell-intrinsic and immune-evasive programs.

    Evidence ChIP-seq, RNA-seq, CARM1 inhibitors, TNBC xenograft, cytotoxic T cell infiltration analysis

    PMID:34865122

    Open questions at the time
    • Whether BRD4 reads the methyl mark directly or indirectly unknown
    • Patient stratification by me-BAF155 status not prospectively validated
  12. 2023 High

    Identification of RNF138 as the E3 ligase that K48-polyubiquitinates SMARCC1 at K643, thereby limiting SWI/SNF occupancy at late inflammatory gene loci, revealed a targeted degradation mechanism that fine-tunes inflammatory transcription kinetics.

    Evidence Co-IP, site-directed mutagenesis of K643, ChIP at inflammatory loci, functional screen

    PMID:36800290

    Open questions at the time
    • Whether RNF138 targets free versus complex-incorporated SMARCC1 unknown
    • Signal that activates RNF138 during inflammation not identified
  13. 2023 High

    Patient-derived SMARCC1 variants that failed to rescue Xenopus knockdown phenotypes causally linked SMARCC1 loss-of-function to human congenital hydrocephalus with aqueductal stenosis and cardiac defects, establishing a Mendelian disease connection.

    Evidence Xenopus morpholino knockdown with patient-variant rescue, human fetal brain RNA-seq

    PMID:38128548

    Open questions at the time
    • Precise chromatin targets in ependymal or neural progenitor cells not mapped
    • Genotype-phenotype correlation across different SMARCC1 variants not established
  14. 2024 High

    Single-nucleus multiomics in hematopoietic stem cells showed that SMARCC1 establishes accessible chromatin at lineage-specifying enhancers (chromatin priming), and its loss impairs neutrophil, B cell, and CD8+ T cell production and creates an immune-suppressive tumor microenvironment.

    Evidence Conditional KO mouse, transplantation, scRNA-seq + ATAC-seq, tumor growth assay

    PMID:39088321

    Open questions at the time
    • Which specific transcription factor motifs are SMARCC1-dependent versus redundant with SMARCC2 not resolved
    • Mechanism of immune-suppressive microenvironment not fully defined
  15. 2025 Medium

    Tissue-specific conditional knockouts revealed additional SMARCC1 roles in OPC differentiation/myelination contributing to ASD-like behavior, in skeletal muscle HIF-1α-dependent glycolytic gene regulation, and in transcription factor partnerships (PRMT1, JUND) at specific loci, underscoring its context-dependent transcriptional functions.

    Evidence OPC-specific and muscle-specific conditional KO mice, ChIP, behavioral assays, metabolic assays, Co-IP

    PMID:37478146 PMID:40270464 PMID:40399563 PMID:41423560

    Open questions at the time
    • Structural basis for SMARCC1's selectivity across different transcription factor partners unknown
    • Whether SMARCC1 versus SMARCC2 has non-redundant roles in each tissue not systematically tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • A complete structural model of SMARCC1 within the assembled BAF complex, the rules governing its differential deployment between BAF/PBAF/ncBAF assemblies, and the interplay between R1064 methylation and K643 ubiquitination in controlling SWI/SNF genomic targeting remain to be determined.
  • Full-length SMARCC1 structure within intact BAF/PBAF not determined
  • Functional redundancy with SMARCC2 not systematically dissected
  • Crosstalk between CARM1 methylation and RNF138 ubiquitination on the same molecule unexplored

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 5 GO:0140110 transcription regulator activity 5 GO:0060090 molecular adaptor activity 3
Localization
GO:0005694 chromosome 4 GO:0005634 nucleus 3
Pathway
R-HSA-1266738 Developmental Biology 5 R-HSA-4839726 Chromatin organization 5 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1643685 Disease 4 R-HSA-168256 Immune System 4 R-HSA-5357801 Programmed Cell Death 4
Partners
BRG1CARM1KPNA2PRMT1RNF138SMARCB1SMARCD1SMARCE1
Complex memberships
PBAFSWI/SNF (BAF)

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 SRG3 (mouse SMARCC1 ortholog) associates with a mouse SWI2 homolog (BRG1) in immunoprecipitation, indicating it is a core component of the mammalian SWI/SNF complex, and is required for glucocorticoid-induced apoptosis in a thymoma cell line (antisense knockdown reduces apoptosis). Immunoprecipitation, antisense RNA knockdown, apoptosis assay The Journal of experimental medicine Medium 9151708
1998 The yeast SMARCC1 ortholog Swh3/Rsc8 directly interacts with Rsc6 (a Swp73/BAF60 homolog) and with Sth1 (the Swi2/Snf2 ATPase), establishing these interactions as forming the structural core of SWI/SNF-related complexes; direct interaction confirmed by in vitro binding of bacterially produced proteins. Two-hybrid, in vitro binding assay with bacterially produced proteins, genetic suppression Nucleic acids research High 9685490
1999 BAF155 and BRG1, mammalian SWI/SNF subunits, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase; BRG1-induced growth arrest and senescence can be overcome by cyclin E overexpression, indicating that cyclin E modulates SWI/SNF activity to maintain a transcriptionally permissive chromatin state. Co-immunoprecipitation, in vitro kinase assay, overexpression growth arrest assay, beta-galactosidase senescence assay Molecular and cellular biology High 9891079
2001 SRG3 (SMARCC1) is essential for early embryogenesis; homozygous null mice degenerate after implantation with inner cell mass failure, and ~20% of heterozygotes develop exencephaly due to failure of neural fold elevation. Gene knockout in mice, embryo outgrowth assay, histological analysis Molecular and cellular biology High 11604513
2001 SRG3 associates with the glucocorticoid receptor (GC receptor) in thymocytes but not in peripheral T cells; transgenic overexpression of SRG3 in peripheral T cells induces formation of the SRG3–GC receptor complex and renders these cells sensitive to GC-induced apoptosis; a dominant-negative SRG3 mutant blocks complex formation and reduces GC sensitivity. Co-immunoprecipitation, transgenic mouse overexpression, dominant-negative mutant, apoptosis assay Journal of immunology High 11441086
2001 Activated Notch1 (NotchIC) down-regulates SRG3 promoter activity and SRG3 expression, thereby conferring resistance to GC-induced apoptosis; transgenic SRG3 overexpression restores GC sensitivity in Notch1-transgenic thymocytes, placing SRG3 downstream of Notch1 in the GC sensitivity pathway. Promoter-reporter assay, transgenic rescue epistasis, apoptosis assay PNAS High 11504912
2004 TCR signaling inhibits SRG3 expression via Ras→MEK/ERK and PI3K pathways by repressing E protein and Ets transcription factor binding to the SRG3 proximal promoter, thereby desensitizing thymocytes to GC-induced apoptosis; promoter mutations at E protein/Ets sites abolish TCR-mediated repression. Pharmacological inhibitors, promoter-reporter assay, site-directed mutagenesis, primary thymocyte apoptosis assay The Journal of biological chemistry High 15016814
2004 E2A/HEB heterodimers bind an E-box element in the SRG3 promoter to activate SRG3 transcription; Id proteins (especially Id3, induced by TCR via MEK/ERK) antagonize this binding and repress SRG3, reducing GC sensitivity; retroviral Id3 overexpression confers GC resistance that is overcome by SRG3 overexpression, placing this axis upstream of SRG3. EMSA, promoter-reporter assay, retroviral transduction, apoptosis assay, ChIP-implied epistasis The Journal of biological chemistry High 15016815
2004 Nitric oxide (NO) protects thymocytes from GC-induced apoptosis by repressing SRG3 transcription through inactivation of Sp1 DNA-binding activity at the SRG3 promoter; forced SRG3 overexpression from a heterologous promoter reverses NO-mediated rescue. EMSA, promoter-reporter assay, Sp1 binding assay, overexpression rescue, apoptosis assay The Journal of biological chemistry Medium 15187086
2005 SRG3 directly interacts with SNF5, BRG1, and BAF60a within the mammalian SWI/SNF complex; the SWIRM domain mediates SRG3–SNF5 interaction and the SANT domain mediates SRG3–BRG1 interaction; SRG3 stabilizes these partners by attenuating their proteasomal degradation, as confirmed in cell lines and in SRG3 transgenic/haploinsufficient mice. Co-immunoprecipitation, domain deletion mapping, proteasome inhibitor assays, SRG3 transgenic and knockout mouse analysis The Journal of biological chemistry High 17255092
2005 BAF155 and BAF170 protein levels dictate the maximum cellular amount of BAF57; exogenous BAF57 expression triggers proteasome-dependent degradation of endogenous BAF57; the interaction between BAF57 and BAF155 (domain-mapped) protects BAF57 from degradation, providing a stoichiometry-maintenance mechanism for the SWI/SNF complex. Co-immunoprecipitation, domain deletion mapping, proteasome inhibitor assay, exogenous expression Molecular and cellular biology High 16199878
2005 SRG3 enhances androgen receptor (AR) transactivation through multiple mechanisms: (1) SRG3 is induced by androgen via AR, creating a positive feedback loop; (2) SRG3 coactivates AR by upregulating SRC-1 protein levels; (3) the AR/SRG3/SRC-1 complex occupies androgen response elements on endogenous gene promoters in vivo; (4) this coactivation is functional even in BRG1/BRM-deficient cells, indicating an SWI/SNF-independent function. Reporter assay, ChIP, co-immunoprecipitation, Western blot, BRG1/BRM-deficient cell line assay Molecular and cellular biology High 15923603
2005 Sp1/Sp3 bind two canonical GC boxes and one non-canonical CCTCCT motif in the SRG3 promoter; Ets family members cooperate synergistically or antagonistically with Sp factors to regulate SRG3 transcription, as shown by Drosophila SL2 cell reporter assays and EMSA. Promoter-reporter assay, EMSA, Drosophila SL2 cell transfection Biochemical and biophysical research communications Medium 16288722
2005 Notch1 confers GC resistance through Deltex1: Deltex1 competitively inhibits p300 binding to E2A/HEB at E-box elements on the SRG3 promoter, repressing SRG3 expression; RBP-J represses SRG3 through an N-box motif; forced Deltex1 expression rescues DP thymocytes from GC-induced apoptosis. Promoter-reporter assay, co-immunoprecipitation, ChIP-implied competition assay, overexpression rescue, apoptosis assay Cell death and differentiation Medium 16341126
2007 SRG3 is required for angiogenesis and visceral endoderm development in the yolk sac; SRG3-deficient (transgene-rescued) embryos show defects in blood vessel formation and reduced expression of angiogenesis-related genes (Angiopoietin1, Tie2, EphrinB2, Ihh, Notch1) in the yolk sac visceral endoderm. Conditional transgene rescue mouse model, gene expression analysis, histology Developmental biology High 18206867
2007 SRG3 is detected in pronuclei of mouse zygotes shortly after fertilization, with higher levels in the male pronucleus than female pronucleus; nuclear accumulation is partially dependent on protein synthesis but not transcription; co-expression with BRG1 and INI1 parallels SP1 and TBP, implicating SWI/SNF in early chromatin function. Immunofluorescence, Western blot, protein synthesis inhibitor (cycloheximide), transcription inhibitor (alpha-amanitin) Zygote Medium 17462105
2009 Smarcc1/Baf155, as part of the PBAF complex, is required for repression of Nanog and other self-renewal genes during mESC differentiation; Smarcc1 knockdown suppresses loss of Nanog even in the absence of Oct4; Smarcc1 expression is necessary for heterochromatin formation and chromatin compaction during differentiation, coupling gene repression with global chromatin structural changes. shRNA functional genetic screen, Nanog promoter reporter, Nanog protein expression, heterochromatin staining, chromatin compaction assay Stem cells High 19785031
2010 Srg3 (mouse SMARCC1) acts as a tumor suppressor: DNA damage signals promote Srg3 degradation via p53 induction; Srg3 deficiency promotes G1 arrest but antagonizes apoptotic response by inducing p53 and p21 proteins; Srg3 heterozygous mice are prone to sarcoma formation enhanced by p53 haploinsufficiency. Gene knockout/heterozygous mouse model, DNA damage assays, Western blot, cell cycle analysis, tumor incidence analysis Oncogene High 20935679
2011 Re-expression of full-length but not truncated BAF155 in BAF155-deficient cancer cell lines (SNUC2B colon carcinoma and SKOV3 ovarian carcinoma) leads to reduced colony formation and replicative senescence, identifying the C-terminal proline-glutamine rich domain as critical for tumor suppressor activity; loss of BAF155 does not affect RB-mediated cell cycle arrest. BAF155 re-expression in null cell lines, colony formation assay, senescence assay, truncation mapping Epigenetics Medium 22139574
2012 CHFR E3 ubiquitin ligase interacts with BRG1, SNF5, and BAF60a and ubiquitinates them for proteasomal degradation; SRG3/mBAF155 stabilizes these components by blocking their interaction with CHFR, providing the molecular mechanism for SRG3-mediated complex stabilization. Co-immunoprecipitation, ubiquitination assay, proteasome inhibitor assay, Western blot Biochemical and biophysical research communications Medium 22285184
2013 Wwp2, a HECT-domain E3 ubiquitin ligase, interacts with SRG3 via its WW domain binding the PPPY motif of SRG3, promotes SRG3 K48-linked ubiquitination and proteasomal degradation; catalytically inactive Wwp2 mutant abolishes SRG3 ubiquitination. Co-immunoprecipitation, ubiquitination assay, catalytically inactive mutant, proteasome inhibitor Biochemical and biophysical research communications Medium 24365151
2014 CARM1 methylates BAF155 (SMARCC1) at arginine R1064; this methylation directs methylated BAF155 to unique chromatin regions including c-Myc pathway gene loci, regulating breast cancer cell migration and metastasis; identified using CARM1 knockout cell lines (ZFN technology) as a substrate discovery platform. Zinc-Finger Nuclease CARM1 knockout, mass spectrometry substrate identification, ChIP-seq, methylation-specific antibody, migration assay Cancer cell High 24434208
2014 A missense allele of Baf155 (Baf155msp3) causes highly penetrant exencephaly in homozygous mice due to proliferation and apoptosis defects in the neural tube; RNA-Seq reveals few but variable gene expression changes in neural tissue, suggesting inconsistent gene regulation contributes to neural tube closure failure. ENU mutagenesis, homozygous mutant mouse, RNA-Seq, histological analysis of proliferation/apoptosis Developmental neurobiology Medium 24170322
2017 Crystal structure of the BAF155 SWIRM domain in complex with the BAF47 RPT1 domain reveals that SWIRM is a modular interaction domain for BAF47, functionally distinct from other SWIRM domains that bind DNA; extensive mutagenesis and ITC/NMR confirmed the interface. X-ray crystallography, ITC, NMR titration, mutagenesis Journal of molecular biology High 28438634
2018 BAF155 is required for normal PAX6 transcriptional activity in cortical progenitors; conditional BAF155 deletion leads to reduced basal intermediate progenitor (bIP) pool, increased basal radial glia via apical RG delamination, reduced expression of bIP specification genes and CDC42 effector CEP4 (in a PAX6-dependent manner), implicating BAF155-dependent chromatin remodeling in cortical progenitor genesis. Conditional knockout mouse, immunostaining, gene expression analysis, ChIP-implied PAX6 functional epistasis iScience Medium 30240734
2019 RBM15, a subunit of the m6A methyltransferase complex, interacts with BAF155 mRNA and mediates its degradation through the mRNA methylation machinery (METTL3-dependent); RBM15 ablation increases BAF155 expression, RBM15 overexpression decreases BAF155 mRNA and protein and perturbs BAF155-dependent transcriptional activity and apical RG delamination in developing cortex. RIP assay (RNA immunoprecipitation), overexpression/knockdown in cells and in vivo, mRNA stability assay, in utero electroporation Molecular neurobiology Medium 31020615
2019 BAF155 protects HBx protein from ubiquitin-independent proteasomal degradation by competing with the 20S proteasome subunit PSMA7 for binding to HBx; the BAF155 SANT domain directly binds HBx residues 81-120; BAF155 expression increases HBx steady-state levels and enhances HBx transactivation function. Co-immunoprecipitation, domain deletion mapping, siRNA knockdown, Western blot, reporter assay Emerging microbes & infections Medium 31533543
2020 Crystal structure and NMR of the hSNF5 RPT1/BAF155 SWIRM complex reveals that hSNF5 undergoes a coil-to-helix transition upon binding, forming a new αN helix that interacts with the β2-α1 loop of hSNF5 and hydrophobically contacts BAF155 SWIRM; the N-terminal loop region of hSNF5 is critical for BAF155 interaction and is mutated in Rhabdoid tumors. X-ray crystallography, NMR spectroscopy, multi-angle light scattering, biophysical binding assays International journal of molecular sciences High 32244797
2021 Methylated BAF155 (me-BAF155, CARM1-mediated R1064 methylation) promotes tumor metastasis by two mechanisms: (1) activating super-enhancer-addicted oncogenes by recruiting BRD4, and (2) repressing interferon α/γ pathway genes to suppress host immune response; CARM1 inhibition abrogates oncogene expression and boosts cytotoxic T cell tumor infiltration. ChIP-seq, RNA-seq, CARM1 inhibitors, TNBC cell migration assay, in vivo xenograft, me-BAF155 antibody staining of CTC Nucleic acids research High 34865122
2021 N-terminus of BAF155/SMARCC1 contains a MarR-like putative DNA-binding domain, a chromodomain (which has lost canonical methylated-lysine binding due to interdomain contacts), and a BRCT domain that together form a distinct structural module; two highly-conserved pockets at the domain cleft represent a potential small-molecule binding site. NMR structure determination, functional mutagenesis analysis of cancer-associated missense mutations, computational pocket analysis Communications biology High 33953332
2022 SMARCC1 enters the nucleus via importin KPNA2 together with nuclear pore proteins Nup50 and Nup153; knockdown of KPNA2, Nup50, or Nup153 reduces nuclear SMARCC1 and increases cytoplasmic SMARCC1; nuclear SMARCC1 promotes bladder cancer cell proliferation and inhibits apoptosis. Co-immunoprecipitation, immunofluorescence, siRNA knockdown, cell cycle analysis, apoptosis assay Frontiers in molecular biosciences Medium 35669562
2022 Co-expression studies define BAF complex core assembly: SMARCC1 C-terminal region (862-966) interacts directly with SMARCE1 (BAF57) residues 210-284, and SMARCC1 (447-966) interacts with SMARCD1 (BAF60a) residues 129-471; crystals of the SMARCC1/SMARCE1 binary complex obtained at 3.2 Å resolution. Co-expression, protein purification, crystallography Biochemical and biophysical research communications Medium 35158202
2023 RNF138, a nuclear E3 ubiquitin ligase, interacts with SMARCC1 and mediates its K48-linked polyubiquitination at Lys643, targeting it for proteasomal degradation; RNF138-mediated SMARCC1 degradation inhibits chromatin remodeling at SWI/SNF-regulated late inflammatory gene loci, fine-tuning the kinetics of inflammatory gene transcription. Co-immunoprecipitation, ubiquitination assay with K48-linkage identification, site-directed mutagenesis (K643), functional screen, ChIP at inflammatory gene loci, gene expression analysis Cell reports High 36800290
2023 SMARCC1 loss-of-function in Xenopus recapitulates human congenital hydrocephalus (aqueductal stenosis and cardiac defects); patient-specific SMARCC1 variants fail to rescue Xenopus knockdown phenotype while wild-type SMARCC1 rescues; hydrocephalic SMARCC1-mutant human fetal brain shows altered expression of neurogenesis transcription factors NEUROD2 and MAB21L2. Xenopus morpholino knockdown, patient-specific variant rescue, optical coherence tomography, in situ hybridization, immunofluorescence, RNA-seq of human fetal brain Brain High 38128548
2023 Baf155 modulates DNA-binding activity of HIF-1α to promoters of its target glycolytic genes in skeletal muscle; muscle-specific Baf155 ablation increases oxidative metabolism, reduces lactate production during exercise, raises ATP levels, and enhances endurance; Baf155 forms a coactivator complex with phospho-STAT3 (pSTAT3) and HIF-1α at target gene promoters. Muscle-specific conditional knockout mouse, ChIP analysis, metabolic assays, exercise capacity testing, Western blot PLoS biology High 37478146
2024 Baf155 in hematopoietic stem and progenitor cells (HSPCs) establishes accessible chromatin at enhancers containing binding motifs for hematopoietic lineage transcription factors (chromatin priming); Baf155-deficient HSPCs produce fewer neutrophils, B cells, and CD8+ T cells, fail hematopoietic regeneration upon transplantation/5-FU injury, and create a more immune-suppressive tumor microenvironment. Conditional knockout mouse, transplantation assay, single-nucleus multiomics (scRNA-seq + ATAC-seq), HSPC lineage tracing, tumor growth assay Cell reports High 39088321
2024 IRF1 transcriptionally activates SMARCC1 expression by recruiting histone modification enzymes GCN5 (H3K27ac writer) and SETD2 (H3K4me3 writer) to the SMARCC1 promoter and upstream region; GCN5 or SETD2 overexpression restores SMARCC1 expression and exacerbates OA-like symptoms; IRF1 and SMARCC1 knockdown reduces IL-1β-induced pro-inflammatory effects in chondrocytes. ChIP assay, overexpression/knockdown, in vivo rat OA model, macrophage polarization assay Journal of orthopaedic translation Medium 38586591
2025 SMARCC1 activates FLOT1 transcription by binding to the FLOT1 promoter; SMARCC1 knockdown reduces macrophage recruitment and M2 polarization, increases ferroptosis (decreased GSH:GSSG ratio, increased lipid peroxidation), and inhibits tumor growth; FLOT1 overexpression rescues the SMARCC1-knockdown phenotype, placing SMARCC1 upstream of FLOT1 in immune evasion and ferroptosis resistance. ChIP assay (SMARCC1 binding to FLOT1 promoter), knockdown, FLOT1 overexpression rescue, macrophage co-culture, xenograft, TEM for ferroptosis Journal of molecular medicine Medium 40108025
2025 PRMT1 recruits the SWI/SNF complex via direct interaction with SMARCC1 (in a methyltransferase-independent manner) to activate IGF2BP2 transcription, promoting carboplatin resistance; conditional PRMT1 knockout reduces tumorigenesis and restores carboplatin sensitivity in vivo. Co-immunoprecipitation, conditional KO mouse, patient-derived organoids, xenograft, gene expression analysis Advanced science Medium 40270464
2025 BAF155 is highly expressed in committed OPCs in mice and regulates OPC differentiation and myelination by coordinating expression of synapse-related genes that mediate OPC-neuron synaptic communication; varying chromatin regulatory roles of BAF155 across brain regions lead to local myelin deficits contributing to ASD-like behavioral deficits. Conditional knockout mouse (OPC-specific), single-cell transcriptomics, behavioral assays, myelin staining Nature communications Medium 41423560
2025 SMARCC1 collaborates with transcription factor JUND at the TIMP1 promoter in COVID-19 monocytes; 7α,25-OHC enhances SMARCC1-JUND interaction and promotes SMARCC1 co-localization with H3K27ac at the TIMP1 locus to activate TIMP1 expression; demonstrated by Co-IP and ChIP-qPCR. Co-immunoprecipitation, ChIP-qPCR, scRNA-seq/scATAC-seq analysis, in vitro 7α,25-OHC treatment Cellular and molecular life sciences Medium 40399563

Source papers

Stage 0 corpus · 65 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 202 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) 124 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 98 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
2019 RBM15 Modulates the Function of Chromatin Remodeling Factor BAF155 Through RNA Methylation in Developing Cortex. Molecular neurobiology 48 31020615
2011 Identification of a core member of the SWI/SNF complex, BAF155/SMARCC1, as a human tumor suppressor gene. Epigenetics 47 22139574
2023 Irf7 regulates the expression of Srg3 and ferroptosis axis aggravated sepsis-induced acute lung injury. Cellular & molecular biology letters 44 37946128
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
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 MicroRNA-202-5p functions as a tumor suppressor in colorectal carcinoma by directly targeting SMARCC1. Gene 31 30144500
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
1998 Direct interaction between Rsc6 and Rsc8/Swh3,two proteins that are conserved in SWI/SNF-related complexes. Nucleic acids research 29 9685490
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 25 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 20 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
2020 The Arabidopsis zinc finger proteins SRG2 and SRG3 are positive regulators of plant immunity and are differentially regulated by nitric oxide. The New phytologist 16 33037639
2022 Capecitabine Regulates HSP90AB1 Expression and Induces Apoptosis via Akt/SMARCC1/AP-1/ROS Axis in T Cells. Oxidative medicine and cellular longevity 15 35368874
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
2024 A novel SMARCC1 BAFopathy implicates neural progenitor epigenetic dysregulation in human hydrocephalus. Brain : a journal of neurology 14 38128548
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
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
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 10 22285184
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
2004 Nitric oxide inhibits glucocorticoid-induced apoptosis of thymocytes by repressing the SRG3 expression. The Journal of biological chemistry 7 15187086
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 6 16288722
2025 SMARCC1 promotes M2 macrophage polarization and reduces ferroptosis in lung cancer by activating FLOT1 transcription. Journal of molecular medicine (Berlin, Germany) 5 40108025
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
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) 3 40270464
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
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