| 2004 |
Baf60c (SMARCD3) is expressed specifically in heart and somites in the early mouse embryo and mediates physical interactions between cardiac transcription factors (GATA4, Tbx5) and the BAF complex ATPase Brg1, thereby potentiating activation of cardiac target genes; silencing causes defects in anterior/secondary heart field expansion and cardiac/skeletal muscle differentiation. |
RNA interference in mouse embryos, cell culture overexpression, co-immunoprecipitation with Brg1 and cardiac transcription factors |
Nature |
High |
15525990
|
| 2003 |
BAF60c1 and BAF60c2 isoforms physically interact with multiple nuclear receptors and transcription factors, are localized primarily in the cell nucleus, and enhance transcriptional activity of PPARγ and RORα1 in a ligand-independent manner by serving as an anchoring point for SWI/SNF complex recruitment. |
Yeast two-hybrid screen, co-immunoprecipitation, subcellular fractionation/localization, transcriptional reporter assays |
The Journal of biological chemistry |
High |
14701856
|
| 2011 |
BAF60c pre-assembles with MyoD on regulatory elements of MyoD-target genes in myoblasts prior to transcription; p38α kinase phosphorylates BAF60c on a conserved threonine in response to differentiation signals, promoting incorporation of the MyoD-BAF60c complex into a Brg1-based SWI/SNF complex that remodels chromatin and activates muscle gene transcription. |
ChIP, co-immunoprecipitation, phosphorylation assays with p38α kinase, siRNA knockdown with transcriptional readouts, mutagenesis of threonine phosphorylation site |
The EMBO journal |
High |
22068056
|
| 2007 |
Baf60c is required for Notch-dependent transcriptional activation and functions to stabilize interactions between activated Notch (NICD) and its DNA-binding partner RBP-J; Brg1 is also required, indicating BAF complexes are key components of nuclear Notch signaling and are essential for establishing left-right asymmetry via Nodal activation at the node. |
Baf60c knockdown in mouse embryos (RNAi) and zebrafish, cell culture Notch transcription reporter assays, co-immunoprecipitation of Baf60c with NICD and RBP-J |
Proceedings of the National Academy of Sciences of the United States of America |
High |
17210915
|
| 2012 |
In response to insulin, BAF60c is phosphorylated at S247 by atypical PKCζ/λ, causing translocation from cytoplasm to nucleus; nuclear BAF60c then directly interacts with phosphorylated/acetylated USF-1 to form the lipoBAF complex, which remodels chromatin and activates lipogenic genes (fatty acid synthase, GPAT), increasing triglyceride levels in vivo. |
In vitro kinase assay with PKCζ/λ, subcellular fractionation, co-immunoprecipitation (BAF60c-USF-1), ChIP, mutagenesis of S247, transgenic mouse overexpression |
Molecular cell |
High |
23219531
|
| 2013 |
Baf60c (Smarcd3) in skeletal muscle promotes a switch from oxidative to glycolytic myofiber type by inducing Deptor expression through the Baf60c-Six4 transcriptional complex; Deptor then mediates activation of Akt and glycolytic metabolism in a cell-autonomous manner, protecting mice from diet-induced insulin resistance. |
Muscle-specific transgenic overexpression, muscle-specific knockout, metabolic phenotyping, co-immunoprecipitation (Baf60c-Six4), siRNA knockdown of Deptor, Akt phosphorylation assays |
Nature medicine |
High |
23563706
|
| 2013 |
SMARCD3/Baf60c expression in epithelial cells induces EMT by upregulating Wnt5a expression; RNAi knockdown of Wnt5a or use of blocking antibody reversed Smarcd3-induced EMT, placing Wnt5a downstream of SMARCD3 in this pathway. |
RNAi screen, gain- and loss-of-function in breast cancer cell lines, Wnt5a RNAi and blocking antibody rescue experiments, EpCAM/E-cadherin flow cytometry |
Molecular and cellular biology |
Medium |
23716599
|
| 2013 |
Nodal inhibition by Cerberus-1 induces Baf60c expression in multipotent cardiac progenitors (KDR/Flk1+); Baf60c interacts with GATA4 and Tbx5 to direct SWI/SNF complex (via Brg1) to cardiomyogenic loci, mediating developmental opening of chromatin at the Nkx2.5 cardiac enhancer; overexpression of Baf60c rescued Cer1 or Brg1 siRNA-induced deficits, placing Baf60c downstream of Cer1. |
siRNA knockdown, ATAC/chromatin accessibility assay at Nkx2.5 enhancer, overexpression rescue, co-immunoprecipitation (Baf60c-GATA4/Tbx5), embryonic stem cell cardiomyogenesis model |
Genes & development |
High |
24186978
|
| 2007 |
In zebrafish, Smarcd3 physically interacts with the T-box transcription factor No tail (Ntl/Brachyury), and Smarcd3 overexpression fails to rescue myod expression in ntl mutants; Smarcd3b is the limiting factor that regulates the onset of myogenesis (myod/myf5 expression) downstream of Fgf and Ntl signaling. |
Co-immunoprecipitation (Smarcd3-Ntl), overexpression in zebrafish embryos, ntl mutant epistasis analysis, in situ hybridization for myod/myf5 |
The Journal of biological chemistry |
Medium |
18056260
|
| 2007 |
BAF60c1 and BAF60c2 physically interact with retinoic acid receptors (RARs) and act as coactivators; this coactivating activity is dependent on SRC1 (a HAT coactivator), demonstrating cooperation between SWI/SNF and histone acetyltransferase complexes in RAR-mediated transcription. |
Co-immunoprecipitation, transcriptional reporter assays, SRC1 knockdown epistasis |
Molecular and cellular endocrinology |
Medium |
17363140
|
| 2008 |
Baf60c is a component of a neural progenitor-specific BAF complex; its overexpression in retinal progenitors keeps them in a proliferative state through interaction with the Notch pathway, and Baf60c expression is lost upon neural differentiation but re-expressed in Müller glia that re-enter the cell cycle. |
Immunofluorescence and expression analysis in mouse/human retina, overexpression in retinal progenitors with proliferation readout, Notch pathway interaction assays |
Developmental dynamics |
Medium |
18816825
|
| 2012 |
TGFβ1 activates Baf60c transcription via direct binding of SMAD2/3 complexes to the Baf60c promoter; Baf60c then regulates smooth muscle cell (SMC) gene expression through interaction with SRF at CArG box-containing promoter elements; Baf60c knockdown decreases SMC gene expression while ectopic expression is sufficient to commit progenitor cells to SMC fate in the absence of exogenous cytokines. |
ChIP (SMAD2/3 at Baf60c promoter, Baf60c at SMC gene promoters), co-immunoprecipitation (Baf60c-SRF), siRNA knockdown, overexpression, in vivo vessel contribution assay |
PloS one |
Medium |
23110084
|
| 2014 |
Proinflammatory cytokine TNF-α downregulates Baf60c and Deptor in skeletal muscle via ERK activation; ERK inhibition (U0126) rescues Baf60c and Deptor expression and lowers blood glucose in obese mice; transgenic Baf60c rescue in muscle restores Deptor expression and Akt phosphorylation, linking meta-inflammation to the Baf60c/Deptor/Akt pathway. |
ERK inhibitor treatment of myotubes and obese mice, transgenic overexpression rescue, Akt phosphorylation western blot, blood glucose measurement |
Diabetes |
Medium |
24458360
|
| 2022 |
In vascular smooth muscle cells, BAF60c preserves contractile phenotype by strengthening SRF association with coactivator P300 and the SWI/SNF complex; suppresses NF-κB target gene inflammation by promoting a repressive chromatin state; and prevents apoptosis through transcriptional activation of KLF5-dependent BCL2 expression. VSMC-specific Baf60c knockout aggravated AAA formation in mice. |
VSMC-specific Cre-lox knockout, co-immunoprecipitation (SRF-P300-SWI/SNF), ChIP for repressive chromatin marks at NF-κB targets, ChIP for KLF5/BCL2 locus, angiotensin II and elastase AAA models |
The Journal of clinical investigation |
High |
36066968
|
| 2023 |
SMARCD3 regulates DAB1-mediated Reelin signaling in Purkinje cell migration and medulloblastoma metastasis by orchestrating cis-regulatory elements at the DAB1 locus; increased SMARCD3 activates Reelin-DAB1-Src kinase signaling; EZH2 and NFIX coordinate at the SMARCD3 locus chromatin hub to control SMARCD3 expression. |
Integrated genomic/epigenomic analysis, ChIP-seq, ATAC-seq, in vivo mouse models, Src kinase inhibitor treatment |
Nature cell biology |
Medium |
36849558
|
| 2023 |
Myofiber Baf60c interacts with Six4 to synergistically suppress myocyte Dkk3 expression; myofiber-specific ablation of Baf60c upregulates secreted Dkk3, which inhibits muscle stem cell differentiation and attenuates muscle regeneration; Dkk3 blockade or Baf60c transgenic expression promotes muscle regeneration. |
Myofiber-specific Cre-lox knockout and transgenic overexpression, co-immunoprecipitation (Baf60c-Six4), ChIP at Dkk3 locus, in vivo muscle regeneration assays, Dkk3 knockdown rescue |
The Journal of experimental medicine |
High |
37284884
|
| 2025 |
Baf60c physically interacts with the transcription factor Mef2c and modulates chromatin accessibility at proximal promoter regions upstream of the Musclin gene TSS, negatively regulating Musclin expression in skeletal muscle; muscle-specific Baf60c ablation elevates Musclin and inhibits adipose tissue thermogenesis, while overexpression increases thermogenesis via Musclin-mediated muscle-fat crosstalk. |
Muscle-specific Cre-lox knockout and transgenic overexpression, co-immunoprecipitation (Baf60c-Mef2c), ATAC-seq at Musclin promoter, in vivo metabolic assays (thermogenesis, glucose metabolism) |
Life metabolism |
High |
40585527
|
| 2026 |
BAF60C forms an RNA-protein complex with nucleophosmin (NPM1) and Reg3b mRNA to modulate Reg3b mRNA decay (a non-canonical role distinct from chromatin remodeling); β cell-specific BAF60C deletion aggravates nucleolar stress and islet inflammation by reducing REG3B expression and secretion, impairing β cell-macrophage crosstalk in type 2 diabetes. |
β cell-specific Cre-lox knockout and overexpression, RNA immunoprecipitation (BAF60C-NPM1-Reg3b mRNA complex), mRNA stability assays, co-immunoprecipitation (BAF60C-NPM1), islet inflammation and glucose homeostasis assays |
Developmental cell |
High |
41806831
|
| 2016 |
Knockdown of Smarcd3/Bap60 (Drosophila ortholog) in endothelial cells increases NF-κB-dependent inflammatory signaling; in mammalian aortic endothelial cells exposed to oscillatory shear stress, smarcd3 expression is reduced and siRNA knockdown of smarcd3 induces endothelial inflammation, identifying it as a mechanosensitive anti-inflammatory gene. |
Drosophila RNAi screen (NF-κB reporter readout), siRNA knockdown in mammalian aortic endothelial cells with inflammatory marker readout, oscillatory shear stress in vitro |
Scientific reports |
Medium |
27819340
|
| 2023 |
In cervical cancer, the lncRNA UCA1 promotes SMARCD3 ubiquitination and proteasomal degradation, reducing SMARCD3 protein stability; UCA1-SMARCD3 protein interaction was identified by RNA pull-down and RIP, and ubiquitination assays confirmed UCA1-promoted SMARCD3 degradation. |
RNA pull-down, RNA immunoprecipitation, ubiquitination assays, co-immunoprecipitation, gain- and loss-of-function in cell lines and xenografts |
Molecular carcinogenesis |
Medium |
38116886
|
| 2020 |
BAF60C loss in cardiomyocytes leads to cell cycle defects (increased endoreplication, accumulation of p21 without cell cycle arrest) and unrepaired DNA damage accumulation, identifying SMARCD3 as a regulator of cell cycle checkpoint integrity. |
siRNA knockdown in ER+ breast cancer cells, flow cytometry (cell cycle analysis), immunofluorescence (p21, DNA damage markers), microscopy |
Breast cancer research and treatment |
Medium |
33180234
|