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72 results for “TEAD”
Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis "
<table> <tbody> <tr> <td> <p>Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease characterized by excessive extracellular matrix (ECM) deposition. Current IPF therapies slow disease progression but do not stop or reverse it. The (myo)fibroblasts are thought to be the main cellular contributors to excessive ECM production in IPF. Here we report that fibrotic AT2 cells regulate production and crosslinking of ECM via the co-transcriptional activator YAP. YAP leads to increase expression of Lysyloxidase (LOX) and subsequent LOX mediated crosslinking by fibrotic AT2 cells. Pharmacological YAP inhibition reverses fibrotic AT2 cell reprogramming and LOX expression in experimental lung fibrosis <span>in vivo</span><span> and in human fibrotic </span><span>tissue ex vivo</span><span>. We thus identify YAP-TEAD/LOX inhibition in AT2 cells as a promising potential new therapy for IPF patients.<span> </span></span></p> <p><span><span>In</span></span></p> </td> </tr> </tbody> </table>
Data from: Covalent disruptor of YAP-TEAD association suppresses defective Hippo signaling
<p>The transcription factor TEAD, together with its coactivator YAP/TAZ, is a key transcriptional modulator of the Hippo pathway. Activation of TEAD transcription by YAP has been implicated in a number of malignancies, and this complex represents a promising target for drug discovery. Here, we employed covalent fragment screening approach followed by structure-based design to develop an irreversible TEAD inhibitor MYF-03-69. Using a range of <em>in vitro</em> and cell-based assays we demonstrated that through a covalent binding with TEAD palmitate pocket, MYF-03-69 disrupts YAP-TEAD association, suppresses TEAD transcriptional activity and inhibits cell growth of Hippo signaling defective malignant pleural mesothelioma (MPM). Further, a cell viability screening with a panel of 903 cancer cell lines indicated a high correlation between TEAD-YAP dependency and the sensitivity to MYF-03-69.</p> <p>To validate MYF-03-69 as potent and selective pan-TEAD inhibitor, we interrogated the proteome-wide selectivity profile of MYF-03-69 on cysteine labeling using a streamlined cysteine activity-based protein profiling (SLC-ABPP) approach and generated the spreadsheet "Supplementary_Dataset_1._Proteome-wide_selectivity_profile_of_MYF-03-69_on_cysteines_labeling_using_SLC-ABPP_approach". We employed the cysteine reactive desthiobiotin iodoacetamide (DBIA) probe which was reported to map more than 8,000 cysteines and performed a competition study on NCI-H226 cells pretreated with 0.5, 2, 10 or 25 µM of MYF-03-69 for 3 hours in triplicate. The cysteines that were conjugated >50% (competition ratio CR>2) compared to DMSO control were analyzed and assigned to the protein targets. In the DMSO control group, although DBIA mapped 12,498 cysteines in total, the TEAD PBP cysteines were not detected. This might be due to low TEAD1-4 protein abundance and/or inability of the PBP cysteines to be labeled given that they are mostly modified by palmitate under physiological conditions. Among 12,498 mapped cysteines, only 7 cysteines were significantly labeled (i.e. exhibited >50% conjugation or CR>2) by 25 µM of MYF-03-69, and all of these sites exhibited dose-dependent engagement.</p> <p>To study the whole transcriptome perturbation by TEAD inhibitor MYF-03-69, mRNA sequencing was performed in NCI-H226 cells that were treated with 0.1 μM, 0.5 μM, and 2 μM of MYF-03-69 and generated the spreadsheet "Supplementary_Dataset_2._List_of_differentially_expressed_genes_under_MYF-03-69_treatments". The genes that were differentially expressed with statistical significance (Fold change > 1.5 and adjusted p value < 0.05) are listed in this dataset.</p> <p>To investigate whether TEAD inhibition by MYF-03-69 was selectively lethal to YAP/TEAD-dependent cancers, PRISM screening across a broad panel of cell lineages were performed and generated the spreadsheet "Supplementary_Dataset_3". 903 cancer cells were treated with TEAD inhibitor MYF-03-69 for 5 days. The viability values were measured at 8-point dose manner (3-fold dilution from 10 μM) and fitted a dose-response curve for each cell line. Area under the curve (AUC) was calculated as a measurement of compound effect on cell viability. CERES score of YAP1 or TEADs from CRISPR (Avana) Public 21Q1 dataset (DepMap) were listed in the spreadsheet and used to estimate gene-dependency. The CERES Score of most dependent TEAD isoform was used to represent TEAD dependency. With PRISM screen dataset of TEAD inhibitor MYF-03-69, we investigated whether TEAD inhibition recapulates genetically knockout outcome of YAP or TEADs and generated the spreadsheet "Supplementary_Dataset_4". Correlation analysis between compound PRISM sensitivity (log2.AUC of each cell line) and dependency of certain gene (CRISPR knockout score for each cell line, from DepMap Public 20Q4 Achilles_gene_effect.csv dataset) across the PRISM cell line panel. The Pearson correlation coefficients and associated p-values were computed. Positive correlations correspond to dependency correlating with increased sensitivity. The q-values (a corrected significance value accounting for false discovery rate) are computed from p-values using the Benjamini Hochberg algorithm. Associations with q-values above 0.1 are filtered out. This correlation analysis reveals that the dependency scores of TEAD1 and YAP1 according to genomic knockout dataset (DepMap portal) provided the highest correlation with the compound PRISM sensitivity profile. This is followed by TP53BP2, a gene that is also involved in Hippo pathway as activator of TAZ.</p>
Data from: Covalent disruptor of YAP-TEAD association suppresses defective Hippo signaling
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Next Generation Sequencing Quantitative Analysis of TEAD Inhibitors in NCI-H226 cells
GEO Series GSE215114. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Decoding the regulatory landscape of melanoma reveals TEADS as regulators of the invasive cell state.
GEO Series GSE60664. Homo sapiens. 17 samples. Type: Expression profiling by high throughput sequencing.
Cooperation between the Hippo and MAPK pathway activation drives acquired resistance to TEAD inhibition III
GEO Series GSE246583. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing.
Next Generation Sequencing Quantitative Analysis of TEAD Palmitoylation Inhibitor MGH-CP1 in Breast Cancer Cell Line
GEO Series GSE140396. Homo sapiens. 4 samples. Type: Expression profiling by high throughput sequencing.
A novel irreversible TEAD inhibitor, SWTX-143, blocks the Hippo pathway and causes tumor regression in preclinical mesothelioma models [SubQ]
GEO Series GSE222962. Homo sapiens. 24 samples. Type: Expression profiling by high throughput sequencing.
Cooperation between the Hippo and MAPK pathway activation drives acquired resistance to TEAD inhibition IV
GEO Series GSE246590. Homo sapiens. 2 samples. Type: Other.
A novel irreversible TEAD inhibitor, SWTX-143, blocks the Hippo pathway and causes tumor regression in preclinical mesothelioma models [Invitro]
GEO Series GSE222960. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Human malignant mesothelioma NCI-H226 cells treated with TEAD inhibitor K-975 in SCID mice.
GEO Series GSE196726. Homo sapiens. 94 samples. Type: Expression profiling by high throughput sequencing.
The YAP-TEAD complex promotes senescent cell survival by lowering endoplasmic reticulum stress
GEO Series GSE221254. Homo sapiens; Mus musculus. 19 samples. Type: Expression profiling by high throughput sequencing.
Cooperation between the Hippo and MAPK pathway activation drives acquired resistance to TEAD inhibition [multiome-seq]
GEO Series GSE247442. Homo sapiens. 3 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
The YAP-TEAD complex promotes senescent cell survival by lowering endoplasmic reticulum stress [bulk RNA-seq]
GEO Series GSE221104. Homo sapiens. 9 samples. Type: Expression profiling by high throughput sequencing.
Convergence of YAP/TAZ, TEAD and P63 activity directs premalignant lung gene expression [RNA-seq]
GEO Series GSE213655. Homo sapiens. 18 samples. Type: Expression profiling by high throughput sequencing.
Identification of YAP-TEAD gene signatures in metastatic melanoma
GEO Series GSE234083. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
The YAP-TEAD complex promotes senescent cell survival by lowering endoplasmic reticulum stress [scRNA-seq]
GEO Series GSE221117. Homo sapiens. 2 samples. Type: Expression profiling by high throughput sequencing.
Specific and redundant roles of TEAD transcription factors in C2C12 cell and primary myoblast differentiation (RNA-Seq)
GEO Series GSE82192. Mus musculus. 24 samples. Type: Expression profiling by high throughput sequencing.
AIB1 and TEAD ChIP-seq
GEO Series GSE137284. Homo sapiens. 7 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
YAP-TEAD signaling promotes Basal Cell Carcinoma development via c-JUN/AP1 axis [RNA-seq]
GEO Series GSE115147. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
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