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New targets of TEAD1 revealed by ChIP-on-chip

ABSTRACT: TEAD1 acts as a key molecule of muscle development, and trans-activates multiple target genes involved in cell proliferation and differentiation pathways. However, its target genes in skeletal muscles, regulatory mechanisms and networks are unknown. Here, we use ChIP-on-chip to identify direct target genes of TEAD1.

ORGANISM(S): Mus musculus

PROVIDER: GSE26107 | GEO | 2011/02/01

SECONDARY ACCESSION(S): PRJNA135185

REPOSITORIES: GEO

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New targets of TEAD1 revealed by ChIP-on-chip

Project description:TEAD1 acts as a key molecule of muscle development, and trans-activates multiple target genes involved in cell proliferation and differentiation pathways. However, its target genes in skeletal muscles, regulatory mechanisms and networks are unknown. Here, we use ChIP-on-chip to identify direct target genes of TEAD1. All animal procedures were performed according to protocols approved by Hubei Province, P. R. China for Biological Studies Animal Care and Use Committee. Skeletal muscle tissues were collected from three adult Kunming mice.

2011-02-01 | E-GEOD-26107 | biostudies-arrayexpress

Analysis of chromatin accessibility uncovers TEAD1 as a regulator of migration in human glioblastoma

Project description:The intrinsic drivers of migration in glioblastoma (GBM) are poorly understood. To better capture the native molecular imprint of GBM and its developmental context, we isolate human stem cell populations from GBM (GSC) and germinal matrix tissues and map their chromatin accessibility via ATAC-seq. We uncover two distinct regulatory GSC signatures, a developmentally-shared/proliferative and a tumor-specific/migratory one in which TEAD1/4 motifs are uniquely overrepresented. Using ChIP-PCR we validate TEAD1 trans occupancy at accessibility sites within EGFR, AQP4, and CDH4. To further characterize TEAD’s functional role in GBM, we knockout TEAD1 or TEAD4 in patient-derived GBM lines using CRISPR-Cas9. TEAD1 ablation robustly diminishes migration, both in vitro and in vivo, and alters migratory and EMT transcriptome signatures with consistent downregulation of its target AQP4. TEAD1 overexpression restores AQP4 expression, and both TEAD1 and AQP4 overexpression rescue migratory deficits in TEAD1-knockout cells, implicating a direct regulatory role for TEAD1-AQP4 in GBM migration.

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TEAD1-DBD-DNA interaction studied by structural MS

Project description:TEAD transcription factors mediate gene expression regulation through interactions with their DNA response M-CAT motif. They are active mainly during growth and development and induce gene expression of proteins involved in cell proliferation, differentiation or apoptosis prevention. TEADs and many of their target proteins are known to be upregulated in several types of cancers. To study the interaction of DNA binding domain of TEAD1 with M-CAT motifs of different orientations originating from regulatory regions of human genes (CTGF, SRF, C-MYC and GLUT1), dissociation constant of each complex was determined using fluorescence anisotropy assay. Structural mass spectrometry techniques (H/D exchange and quantitative chemical cross-linking) and molecular docking were utilized for structural characterization of the binding interface. In-vitro results were correlated with situation in living cells studied by ChIP and Q-PCR.

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YAP1/TEAD1 ChIP in N/TERT2G human keratinocytes

Project description:YAP1/TEAD1 ChIP was performed in N/TERT2G human keratinocytes

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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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YAP1/TEAD1 ChIP in N/TERT2G human keratinocytes

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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 is required to maintain adult cardiomyocyte function

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

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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.

2022-12-14 | GSE139152 | GEO

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