Similar Datasets
Project description:Genome-wide enrichment of YAP and TEAD1 stimulated by lactate
| PRJNA826909 | ENA
Project description:Genome-wide mapping of FOSL1, YAP, TAZ and TEAD1 binding sites in MSK-PCa3 cells
2022-02-17 | GSE196732 | GEO
Project description:ChIP-Seq profiling using human umbilical vein endothelial cells (HUVECs) to identify endogenous YAP, TAZ and TEAD1 DNA binding sites.
2022-05-02 | GSE163458 | GEO
Project description:Genome-wide mapping of FOSL1, YAP, TAZ and TEAD1 binding sites in DU145 cells
2022-02-17 | GSE196733 | GEO
Project description:Regulation of organ size is important for development and tissue homeostasis. In Drosophila, Hippo signaling controls organ size by regulating the activity of a TEAD transcription factor, Scalloped, through modulation of its coactivator protein Yki. The role of mammalian Tead proteins in growth regulation, however, remains unknown. Here we examined the role of mouse Tead proteins in growth regulation. In NIH3T3 cells, cell density and Hippo signaling regulated the activity of Tead proteins by modulating nuclear localization of a Yki homologue, Yap, and the resulting change in Tead activity altered cell proliferation. Tead2-VP16 mimicked Yap overexpression, including increased cell proliferation, reduced cell death, promotion of EMT, lack of cell contact inhibition, and promotion of tumor formation. Growth promoting activities of various Yap mutants correlated with their Tead-coactivator activities. Tead2-VP16 and Yap regulated largely overlapping sets of genes. However, only a few of the Tead/Yapregulated genes in NIH3T3 cells were affected in Tead1-/-;Tead2-/- or Yap-/- embryos. Most of the previously identified Yap-regulated genes were not affected in NIH3T3 cells or mutant mice. In embryos, levels of nuclear Yap and Tead1 varied depending on cell types. Strong nuclear accumulation of Yap and Tead1 were seen in myocardium, correlating with requirements of Tead1 for proliferation. However, their distribution did not always correlate with proliferation. Taken together, mammalian Tead proteins regulate cell proliferation and contact inhibition as a transcriptional mediator of Hippo signaling, but the mechanisms by which Tead/Yap regulate cell proliferation differ depending on cell types, and Tead, Yap and Hippo signaling may play multiple roles in mouse embryos. We used microarrays to know the gene expression profiles regurated by Tead2-VP16, Tead2-EnR, Yap, and cell density in NIH3T3 cells. Keywords: Cell density, genetic modification Tead2-VP16-, Tead2-EnR-, Yap- and control vector-expressing cells were cultured at low or high density for RNA extraction and hybridization on Affymetrix microarrays.
2008-11-20 | E-GEOD-12498 | biostudies-arrayexpress
Project description:The vestigial like family proteins (VGLL) are thought to regulate transcription by interacting with the TEA domain transcription factors (TEAD), the primary mediators of the Hippo pathway. However, the functional regulation of VGLL proteins remains poorly characterized. Here, we explored the molecular mechanism of two VGLL2 and TEAD1 fusion proteins generated by recurrent translocations in spindle cell rhabdomyosarcoma. We demonstrated that, compared to VGLL2 and TEAD1 alone, VGLL2-NCOA2 and TEAD1-NCOA2 act as strong transcriptional activators of TEAD-mediated transcription. Although VGLL2-NCOA2 and Yes1 associated transcriptional regulator (YAP) control overlapping transcriptional programs and chromatin landscapes, the downstream transcription induced by the fusion proteins does not require YAP and WW domain containing transcription regulator 1 (TAZ). Furthermore, VGLL2-NCOA2 and TEAD1-NCOA2 fusions engage distinct epigenetic regulation by recruiting E1A binding protein p300 (p300) to drive TEAD-dependent transcription. We showed that small molecule p300 inhibition can suppress VGLL2-NCOA2 and TEAD1-NCOA2-induced oncogenic transformation both in vitro and in vivo. Overall, our data reveal a tumorigenic mechanism of VGLL and TEAD fusion proteins that is related to the Hippo pathway but independent of YAP/TAZ, suggesting potential therapeutic strategies for tumors carrying VGLL, TEAD, or nuclear receptor coactivator (NCOA) gene rearrangements.
2024-05-22 | GSE260782 | GEO
Project description:YAP is the principle effector of the Hippo signaling pathway; a key regulator of tissue homeostasis whose dysregulation is linked to cancer development. YAP regulation of gene expression is thought to involve the TEAD transcription factor family. Here we show that YAP and TEAD1 binding always co-occurs and is mediated by single as well as double TEAD1 motifs with a particular 3bp spacer (CATTCCNNNCATTCC). This suggests that YAP activity appears exclusively mediated by TEAD1. Despite being characterized as a promoter-binding factor YAP/TEAD actually binds predominantly to enhancers. Moreover we show that YAP is necessary for activity of the linked gene and proper chromatin state of regulated enhancers. These results establish mode of binding and activation of YAP mediated nuclear response of the Hippo pathway by TEAD1 and provide a comprehensive list and a novel class of direct target genes that are regulated distally and could be exploited for cancer therapeutics. Sequencing of ChIP and input samples for YAP1 and TEAD1 transcription factors and H3K27ac histone modification in SF268 glioblastoma cells and for YAP1 transcription factor in NCI-H2052 mesothelioma cells.
2015-08-25 | E-GEOD-61852 | biostudies-arrayexpress
Project description:The vestigial like family proteins (VGLL) are thought to regulate transcription by interacting with the TEA domain transcription factors (TEAD), the primary mediators of the Hippo pathway. However, the functional regulation of VGLL proteins remains poorly characterized. Here, we explored the molecular mechanism of two VGLL2 and TEAD1 fusion proteins generated by recurrent translocations in spindle cell rhabdomyosarcoma. We demonstrated that, compared to VGLL2 and TEAD1 alone, VGLL2-NCOA2 and TEAD1-NCOA2 act as strong transcriptional activators of TEAD-mediated transcription. Although VGLL2-NCOA2 and Yes1 associated transcriptional regulator (YAP) control overlapping transcriptional programs and chromatin landscapes, the downstream transcription induced by the fusion proteins does not require YAP and WW domain containing transcription regulator 1 (TAZ). Furthermore, VGLL2-NCOA2 and TEAD1-NCOA2 fusions engage distinct epigenetic regulation by recruiting E1A binding protein p300 (p300) to drive TEAD-dependent transcription. We showed that small molecule p300 inhibition can suppress VGLL2-NCOA2 and TEAD1-NCOA2-induced oncogenic transformation both in vitro and in vivo. Overall, our data reveal a tumorigenic mechanism of VGLL and TEAD fusion proteins that is related to the Hippo pathway but independent of YAP/TAZ, suggesting potential therapeutic strategies for tumors carrying VGLL, TEAD, or nuclear receptor coactivator (NCOA) gene rearrangements.
2024-05-22 | GSE260783 | GEO
Project description:Human cytomegalovirus (HCMV) infects up to 80% of the world’s population and is linked to serious morbidity in immunocompromised individuals and newborns. Here, using multiple genome-scale assays and computational approaches, we show that HCMV infection leads to widespread changes in chromatin accessibility and chromatin looping, with hundreds of thousands of human genomic regions affected 48 hours after infection. Integrative analyses reveal that HCMV infection perturbs the Hippo signaling pathway by drastically diminishing TEA domain transcription factor 1 (TEAD1) activity. Chromatin immunoprecipitation experiments confirm extensive concordant loss of TEAD1 binding and H3K27ac active histone marks upon infection. TEAD transcription factors are direct effectors of the Hippo signaling pathway, and our data support a position for TEAD1 at the top of a hierarchy involving key developmental pathways with differential expression subsequent to HMCV infection. Known gene targets of TEAD1, including Cellular Communication Network Factor 1 (CCN1) and Thrombospondin 1 (THBS1), are significantly downregulated with HCMV infection, reflecting diminished TEAD1-mediated activity. HCMV infection reduces TEAD1 binding through four distinct mechanisms: closing of TEAD1-bound chromatin, reduction of Yes1 associated transcriptional regulator (YAP1) and phosphorylated YAP (pYAP1) levels, reduction of TEAD1 transcript and protein levels, and alteration of TEAD1 exon-6 usage. Collectively, these comprehensive genome-scale analyses reveal novel mechanisms induced by HCMV infection.
2024-12-06 | GSE254737 | GEO
Project description:Human cytomegalovirus (HCMV) infects up to 80% of the world’s population and is linked to serious morbidity in immunocompromised individuals and newborns. Here, using multiple genome-scale assays and computational approaches, we show that HCMV infection leads to widespread changes in chromatin accessibility and chromatin looping, with hundreds of thousands of human genomic regions affected 48 hours after infection. Integrative analyses reveal that HCMV infection perturbs the Hippo signaling pathway by drastically diminishing TEA domain transcription factor 1 (TEAD1) activity. Chromatin immunoprecipitation experiments confirm extensive concordant loss of TEAD1 binding and H3K27ac active histone marks upon infection. TEAD transcription factors are direct effectors of the Hippo signaling pathway, and our data support a position for TEAD1 at the top of a hierarchy involving key developmental pathways with differential expression subsequent to HMCV infection. Known gene targets of TEAD1, including Cellular Communication Network Factor 1 (CCN1) and Thrombospondin 1 (THBS1), are significantly downregulated with HCMV infection, reflecting diminished TEAD1-mediated activity. HCMV infection reduces TEAD1 binding through four distinct mechanisms: closing of TEAD1-bound chromatin, reduction of Yes1 associated transcriptional regulator (YAP1) and phosphorylated YAP (pYAP1) levels, reduction of TEAD1 transcript and protein levels, and alteration of TEAD1 exon-6 usage. Collectively, these comprehensive genome-scale analyses reveal novel mechanisms induced by HCMV infection.
2024-12-06 | GSE254736 | GEO