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Transciptome analysis of human aortic smooth muscle cells (HASMCs) with BAF60c knockdown

ABSTRACT: HASMCs were transfected with BAF60c siRNA (siBAF60c, 20um) or control siRNA (siControl) for 48 hours, and serum-starved for 24 hours , followed by RNA-sequencing

ORGANISM(S): Homo sapiens

PROVIDER: GSE180584 | GEO | 2022/09/23

REPOSITORIES: GEO

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Genome-wide maps of chromatin state changes in BAF60c deficient human aortic smooth muscle cells (HASMCs)

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2022-09-23 | GSE180583 | GEO

Transciptomic analysis of human aortic smooth muscle cells (HASMCs) with BAF60a knockdown

Project description:We used NGS-derived transcriptome profiling (RNA-seq) to compare the transcriptional difference between human aortic smooth muscle cells (HASMCs) transfected with 30nM siRNA targeting BAF60a (siBAF60a) or non-targeting siRNA (siControl)

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Transciptome analysis of human aortic smooth muscle cells (HASMCs) with 2-hydroxypropyl-β-cyclodextrin (HPbCD) treatment

Project description:HASMCs were treated with HPbCD (10mg/kg) for 24 hours and harvest for RNA sequence.

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Genome-wide maps of chromatin state changes in BAF60a deficient human aortic smooth muscle cells (HASMCs)

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The tRNA derived fragments (tRFs) expression profiles in human aortic smooth muscle cells (HASMCs)

Project description:To explore the potential involvement of tRNA derived fragments (tRFs) in the human aortic vascular smooth muscle cells (HASMCs), we conducted tRFs profiling in three pairs of differentiated HASMCs (treated with PBS) and dedifferentiated HASMCs (treated with PDGF-BB 50 ng/ml) by microarray. Our results showed that tRFs were aberrantly expressed in dedifferentiated HASMCs compared with differentiated HASMCs and provided potential targets for novel insights into VSMC differentiation or vascular remodeling diseases.

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Signal-dependent incorporation of MyoD-BAF60c into Brg1-based SWI/SNF chromatin-remodeling complex

Project description:Tissue-specific transcription factors initiate differentiation toward a specialized cell type by inducing transcription-permissive chromatin modifications at target gene promoters, through the recruitment of the SWI/SNF chromatin-remodeling complex (1, 2). The molecular mechanism that regulates the chromatin re-distribution of SWI/SNF in response to differentiation signals is currently unknown. Here we show that the muscle determination factor MyoD and the SWI/SNF structural sub-unit, BAF60c (SMARCD3), form a complex on the regulatory elements of MyoD-target genes in undifferentiated myoblasts, prior to the activation of gene expression. MyoD-BAF60c complex is devoid of the ATP-dependent enzymatic sub-units Brg1 and Brm, is required for stable MyoD binding to Ebox sequences, and marks the chromatin for signal-dependent recruitment of the SWI/SNF core complex to muscle loci. BAF60c phosphorylation on a conserved threonine by differentiation-activated p38 signalling promotes the incorporation of MyoD-BAF60c into a Brg1-based SWI/SNF complex, which is competent to remodel the chromatin and activates transcription of MyoD-target genes. Our data support an unprecedented two-step model, by which pre-assembled BAF60c-MyoD complex directs the SWI/SNF complex chromatin re-distribution to muscle loci in response to differentiation cues. Differentiation of C2C12 cells individually interfered for BRG1, BAF60B, BAF60C

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SWI/SNF Chromatin-Remodeling Factor Smarcd3/Baf60c Controls Epithelial-Mesenchymal Transition by Inducing Wnt5a Signaling

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2013-08-19 | E-GEOD-40145 | biostudies-arrayexpress

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2014-08-10 | E-GEOD-59383 | biostudies-arrayexpress

Phosphoroteomics analysis of ALK signaling in neuroblastoma cells

Project description:We used mass spectrometry-based proteomics to unravel anaplastic lymphoma kinase (ALK) signaling in the ALK and MYCN amplified neuroblastoma cell line, NB1. We specifically measured the ALK phosphoproteome upon siRNA depletion of ALK and upon ALK inhibition using the ALK-targeting small-molecule inhibitor lorlatinib. For quantitative phosphoproteomics we used a tandem mass tag (TMT)-based approach. Conditions for the TMT 11-plex setup is specified below. For each siRNA depletion experiment, NB1 cells were treated with siRNA (80 nM; as specified below) for 48 hours prior to stimulation with 0.1% DMSO for 30 minutes. For inhibitor treatment, NB1 cells were treated for 30 minutes with either 10 microM or 10 nM lorlatinib. The experimental treatment conditions and TMT11-plex labeling are specified below: 126: siControl replicate 1, 0.1% DMSO 127N: siControl replicate 2, 0.1% DMSO 127C: siControl replicate 3, 0.1% DMSO 128N: siALK sequence 1, 0.1% DMSO 128C: siALK sequence 2, 0.1% DMSO 129N: siALK mix of sequence 1 and 2, 0.1% DMSO 129C: 10 microM lorlatinib replicate 1 130N: 10 microM lorlatinib replicate 2 130C: 10 microM lorlatinib replicate 3 131N: 10 nM lorlatinib replicate 1 131C: 10 nM lorlatinib replicate 2

2018-11-21 | PXD009477 | Pride

SWI/SNF Chromatin-Remodeling Factor Smarcd3/Baf60c Controls Epithelial-Mesenchymal Transition by Inducing Wnt5a Signaling

2013-08-19 | GSE40145 | GEO

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