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Tead1 regulation of β-cells II

ABSTRACT: Tead1 regulation of β-cells II

PROVIDER: PRJNA661551 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12594080.fastq.gz	Fastqsanger.gz
	SRR12594081.fastq.gz	Fastqsanger.gz
	SRR12594082.fastq.gz	Fastqsanger.gz
	SRR12594083.fastq.gz	Fastqsanger.gz
	SRR12594084_1.fastq.gz	Fastqsanger.gz

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Tead1 regulation of β-cells

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Tead1 regulation of β-cells II

Project description:Purpose: The goal of this study is to determine the regulatory role of Tead1 in β-cells by analyzing the Tead1 cistrome and open chromatin in β-cells Methods: Isolated islets from WT C57bl6 mice of 12 weeks of age were flash frozen. For Chip-seq they were fixed with formaldehyde and then after sonication, IP was performed with Anti-Tead1 antibody or the IgG isotype control. For ATAC-seq 100,000 of the frozen nuclei were tagmented. After DNA extraction, library construction, sequencing was performed using Illumina Hi seq2500. Conclusions: Our study represents the first detailed analysis of the Tead1 cistrome in beta cells.

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Tead1 regulation of β-cells

Project description:Purpose: The goal of this study is to determine the regulatory role of tead1 in β-cells by analyzing the transcriptomal changes with Tead1 deletion in β-cells Methods: Isolated islet mRNA profiles of β-cell Tead1 KO mice compared to control floxed mice at 1 year of age were assessed by RNA-seq using Illumina Hiseq2500. The sequence reads that passed quality filters were analyzed at the transcript isoform level using the CLC genomic workbench. qRT-PCR validation was performed using SYBR Green assays Conclusions: Our study represents the first detailed analysis of beta cell transcriptomes following Tead1 deletion in beta cells.

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Project description:This study investigates transcriptional regulation by TES (TEAD1 Epigenetic Silencer, an engineered epigenetic silencer factor targeting the YAP/TAZ-TEAD axis) in SNB19 glioblastoma cells using RNA-seq. TES was engineered by fusing the KRAB domain, the catalytic domain of DNMT3A together with DNMT3L, and the N-terminal 166 amino acids of TEAD1. RNA-seq was performed 48 hours after lentiviral transduction to identify differentially expressed genes upon TES expression compared to GFP control in three biological replicates per condition. TES expression induced widespread transcriptional repression of YAP/TAZ-dependent gene programs, with downregulated genes enriched for cell-cycle regulation and TEAD family transcription factor binding sites.

2026-02-23 | GSE319888 | GEO

Transcriptional regulation by TES and TEAD1 in SNB19 glioblastoma cells: Cut&Tag

Project description:This study uses Cleavage Under Targets and Tagmentation (Cut&Tag) chromatin profiling to map genome-wide binding sites of TES (TEAD1 Epigenetic Silencer, an engineered epigenetic silencer factor consisting of KRAB-hTEAD1(1-166)-DNMT3A/3L with V5 tag) and overexpressed wild-type TEAD1 (HA-tagged) in SNB19 glioblastoma cells. Cut&Tag was performed using the CUTANA protocol (EpiCypher). Three biological replicates were prepared for TES (detected via anti-V5) and TEAD1 (detected via anti-HA), with mouse IgG and rabbit IgG as negative controls. Peak calling identified binding sites for both factors, showing that TES largely preserves the DNA-binding specificity of wild-type TEAD1 while converting it into a transcriptional repressor.

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Transcriptional regulation by TES and TEAD1 in SNB19 glioblastoma cells: Cut&Tag

Project description:Transcriptional regulation by TES and TEAD1 in SNB19 glioblastoma cells: Cut&Tag

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Transcriptional regulation by TES and TEAD1 in SNB19 glioblastoma cells: RNA-seq

Project description:Transcriptional regulation by TES and TEAD1 in SNB19 glioblastoma cells: RNA-seq

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The function of TEAD1 in cardiac fibroblast activation [ChIP-Seq]

Project description:Cardiac fibroblasts (CFs) are the primary cells tasked with extracellar matrix reorganization and significantly associated with heart failure (HF). Previous studies have shown that TEAD1 deficiency deteriorated heart development and homeostasis. However, the role of TEAD1 in fibroblasts during cardiac remodeling was still undiscovered. Our study demonstrated that TEAD1 was upregulated predominently in cardiac fibroblasts in mice 4 weeks after transverse aortic constriction (TAC) and Ang-II infusion. Echocardiographic and histological analyses demonstrated that CFs- and myofibroblasts-specific TEAD1 deficiency ameliorated TAC-induced cardiac remodeling and treatment with TEAD1 inhibitor, VT103, mimiced this phenotypic effect. Mechanistically, RNA-seq analysis , ChIP-Seq analysis identified TEAD1 promotes the fibroblast-to-myofibroblast transition through the Wnt signalling pathway. In conclusion, TEAD1 is an essential regulator of the pro-fibrotic CFs phenotype associated with pathological cardiac remodeling via the BRD4/Wnt4 signalling pathway.

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