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Figure 2 in Obtainment and characterization of digestive aspartic proteases from the fish Caranx hippos (Linnaeus, 1766)
Figure 2. pH and temperature effect on EE acidic proteases. (A) Optimal temperature; (B) Thermal stability; (C) Optimal pH; (D) pH stability.
Predynastic C-Ware Bowl with Hippos
Ceramic bowl from the Egyptian Predynastic depicting four hippopotomi. This type of ceramic is referred to as cross-white lined or C-ware and dates to the Naqada I-early Naqada II period. This specific vessel dates to the Naqada I and is 15 cm in diameter. This vessel is in the collections of the [Petrie Museum of Egyptian Archaeology](https://www.ucl.ac.uk/culture/petrie-museum), University College London. It is accession number UC15337. Created from 158 photographs (Canon EOS Rebel T5i) using Metashape 1.5.1. Photographed in June 2018 with the permission and assistance of the Petrie Museum. Base was unavailable for photography and has been false colored here. Source: Objaverse 1.0 / Sketchfab
Figure 3 in Obtainment and characterization of digestive aspartic proteases from the fish Caranx hippos (Linnaeus, 1766)
Figure 3. Effect of NaCl on the EE acidic proteases.
Figure 1 in Obtainment and characterization of digestive aspartic proteases from the fish Caranx hippos (Linnaeus, 1766)
Figure 1. EE Zymogram.
Table 2 in Obtainment and characterization of digestive aspartic proteases from the fish Caranx hippos (Linnaeus, 1766)
<p><b>Table 2.</b> Effect of enzyme inhibitors and metal ions on the proteolytic activity of EE.</p><table><tbody><tr><th><b>Chemical Agent</b></th><th><b>Residual Activity (%)</b></th><th><b>Inhibition (%)</b></th></tr></tbody><tbody><tr><th>Control</th><td>100 ± 4.19a*</td><td>0</td></tr><tr><th>DTT</th><td>104 ± 3.25b</td><td>0</td></tr><tr><th>Pepstatin A</th><td>0c</td><td>100</td></tr><tr><th>Pb2+</th><td>85 ± 0.10d</td><td>15</td></tr><tr><th>Mg2+</th><td>87 ± 3.35e</td><td>13</td></tr><tr><th>Al3+</th><td>89 ± 1.20f</td><td>11</td></tr><tr><th>Mn2+</th><td>90 ± 2.05g</td><td>10</td></tr><tr><th>K+</th><td>91 ± 2.55h</td><td>9</td></tr><tr><th>Hg2+</th><td>94 ± 0.72i</td><td>6</td></tr><tr><th>Cd2+</th><td>97 ± 2.16j</td><td>3</td></tr><tr><th>Cu2+</th><td>98 ± 5.51k</td><td>2</td></tr><tr><th>Ca2+</th><td>101 ± 1.08l</td><td>0</td></tr></tbody></table>
Table 1 in Obtainment and characterization of digestive aspartic proteases from the fish Caranx hippos (Linnaeus, 1766)
<p><b>Table 1.</b> Purification of acidic digestive proteases from the stomach of <i>C. hippos</i> fish.</p><table><tbody><tr><th><b>Process step</b></th><th><b>*</b> <b>Total Activity (U)</b></th><th><b>Total Protein (mg)</b></th><th><b>Specific activity (mU. <b>mg-</b> 1<b>)</b></b></th><th><b>Purification (fold)</b></th><th><b>Yield (%)</b></th></tr></tbody><tbody><tr><th>Crude Extract</th><td>1,546 ± 50</td><td>3,523± 102</td><td>439</td><td>1</td><td>100</td></tr><tr><th>EE</th><td>764 ± 36</td><td>1,103 ± 75</td><td>693</td><td>1.6</td><td>49.4</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>
Hippo signaling impairs alveolar epithelial regeneration in pulmonary fibrosis
<p>Idiopathic pulmonary fibrosis (IPF) consists of fibrotic alveolar remodeling and progressive loss of pulmonary function. Genetic and experimental evidence indicates that chronic alveolar injury and failure to properly repair the respiratory epithelium are intrinsic to IPF pathogenesis. Loss of alveolar type 2 (AT2) stem cells or mutations that either impair their self-renewal and/or impair their differentiation into AT1 cells can serve as a trigger of pulmonary fibrosis. Recent reports indicate increased YAP activity in respiratory epithelial cells in IPF lungs. Individual IPF epithelial cells with aberrant Yap activation in bronchiolized regions frequently co-express AT1, AT2, conducting airway selective markers and even mesenchymal or EMT markers, demonstrating "indeterminate" states of differentiation and suggesting that aberrant Yap signaling might promote pulmonary fibrosis. Yet, Yap and Taz have recently also been shown to be important for AT1 cell maintenance and alveolar epithelial regeneration after <em>Streptococcus pneumoniae-</em>induced injury. To investigate how epithelial Yap/Taz might promote pulmonary fibrosis or drive alveolar epithelial regeneration, we inactivated the Hippo pathway in AT2 stem cells resulting in increased nuclear Yap/Taz and found that this promotes their alveolar regenerative capacity and reduces pulmonary fibrosis following bleomycin injury by pushing them along the AT1 cell lineage. Vice versa, inactivation of both Yap and Taz or Taz alone in AT2 stem cells impaired alveolar epithelial regeneration and resulted in increased pulmonary fibrosis upon bleomycin injury. Interestingly, inactivation of only Yap in AT2 stem cells promoted alveolar epithelial regeneration and reduced pulmonary fibrosis. Together, these data suggest that epithelial Yap promotes, and epithelial Taz reduces pulmonary fibrosis suggesting that targeting Yap- but not Taz-mediated transcription might help promote AT1 cell regeneration and treat pulmonary fibrosis.</p>
Data from: Covalent disruptor of YAP-TEAD association suppresses defective Hippo signaling
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Hippo signaling impairs alveolar epithelial regeneration in pulmonary fibrosis
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Follicle Activation by Inhibition of the Hippo Pathway
ClinicalTrials.gov study NCT02792569. IPD Sharing: NO. Countries: 1. Publications: 4.
Platelet Rich Plasma Versus Placebo for the Treatment of Greater Trochanteric Pain Syndrome (HiPPO Trial)
ClinicalTrials.gov study NCT03479190. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Home-Initiated Programme to Prepare for Operation (HIPPO) Study
ClinicalTrials.gov study NCT04271553. IPD Sharing: NO. Countries: 1. Publications: 5.
hippo
SciDraw upload
Single cell transcriptomics reveal an essential role for Hippo signaling in cell state transitions during cardiac fibroblast development
GEO Series GSE100861. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Prp19 is an independent prognostic marker and promotes neuroblastoma metastasis by regulating the Hippo-YAP signaling pathway [SK-N-BE(2)]
GEO Series GSE153398. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Cells to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC
GEO Series GSE88861. Homo sapiens. 29 samples. Type: Expression profiling by array; Genome binding/occupancy profiling by high throughput sequencing.
The Hippo pathway kinase LATS1 scaffolds Beclin1 in autophagy regulation in hepatocellular carcinoma
GEO Series GSE117116. Homo sapiens. 9 samples. Type: Expression profiling by high throughput sequencing.
OSBPL3 Drives Colorectal Cancer Progression via Hippo-YAP Signaling and Modulates MEK Inhibitor Sensitivity
GEO Series GSE308083. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
The hippo pathway effector protein YAP modulated resistance to trametinib neuroblastomas with hyperactivated RAS pathway signalling
GEO Series GSE130401. Homo sapiens. 21 samples. Type: Expression profiling by high throughput sequencing.
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