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2,678 results for “cell signalling”
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>
Detection of HER2+ Breast Cancer Cells using Bioinspired DNA-Based Signal Amplification
<p>Circulating tumor cells (CTC) are promising biomarkers for metastatic cancer detection and monitoring progression. However, CTC detection remains challenging due to their low frequency and heterogeneity. Herein, we report a bioinspired approach to detect individual cancer cells, based on a signal amplification cascade using a programmable DNA hybridization chain reaction (HCR) circuits. We applied this approach to detect HER2+ cancer cells using the anti-HER2 antibody (trastuzumab) coupled to initiator DNA eliciting a HCR cascade that leads to a fluorescent signal at the cell surface. At 4°C, this HCR detection scheme resulted in highly efficient, specific and sensitive signal amplification of the DNA hairpins specifically on the membrane of the HER2+ cells in a background of HER2- cells and peripheral blood leukocytes, which remained almost non-fluorescent. The results indicate that this system offers a new strategy that may be further developed toward an in vitro diagnostic platform for the sensitive and efficient detection of CTC.</p>
Simulated movies with gaussian-shaped pHluorin signal intensity on the cell surface
<p>Synthetic data mimicking exocytic events across a wide range of features including normalized intensity, apparent size and decay mean lifetime. Numbers and spatial location of simulated events are randomly distributed over time.</p> <p>Events could have:</p> <p>* positive attribute: single exponential decay</p> <p>* negative attribute: constant signal for a random amount of time, damped sine decay signal +/- spatial displacement</p>
Phylogenomic analysis of cell-surface receptors and downstream signaling components in the plant lineage
<p>Here we identified cell-surface receptors and downstream signaling components from the genomes of 350 plant species. </p><p>Zip file contains:</p><p>Folder 'seqeunces for downstream signaling components' - FASTA and TREE files of the identified downstream signaling components.</p><p>Folder 'sequences for cell-surface receptors' - FASTA and TREE files of the identified cell-surface receptors.</p><p>Folder 'Specific analysis' - Contains specific analysis for the identified cell-surface receptors.</p><p>Subfolder 'ID analysis' - Contains information on ID clusters and motifs analysis in IDs.</p><p>Subfolder 'LRR motif gap analysis' - Contains information on small (10-29 aa) and large (30-90) gaps between LRR motifs in RLPs and RLKs.</p><p>Subfolder 'LRR-RLK & LRR-RLP phylogenetic analysis' - Contains FASTA and TREE files of the specific domain/regions (C3, C3-F, eJM-TM-cJM, and all) in LRR-RLPs and LRR-RLKs. This subfolder also contains the specific amino acid, charge and motif analysis in this region (see C3F-end features.xlsx).</p><p>Protein counts per species file - Contains the total number of each protein family/subfamily in each of the 350 species.</p><p>simpleToFullNames (translator file)- Translator file for the original ID of each gene. </p>
ERK signaling of invasive cells in mammary organoid
<p>Live-cell imaging of HMT3522 T4-2 invasive mammary epithelial cell line, with fluorescent ERKTR cell signaling reporter and nuclear reporter, to extract trajectory pairs of ERKTR to nuclear cross-correlation as a measure of ERK signaling activity. Datasets X and Y capture ERK signaling state at t and t+1 respectively, while test_obs contains test trajectories and inds_test_starts contains the indices of starting times of test trajectories.</p>
Data for: Dysregulation of mTOR signaling mediates common neurite and migration defects in both idiopathic and 16p11.2 deletion autism neural precursor cells
<p>Autism spectrum disorder (ASD) is defined by common behavioral characteristics, raising the possibility of shared pathogenic mechanisms. Yet, vast clinical and etiological heterogeneity suggests personalized phenotypes. Surprisingly, our iPSC studies find that six individuals from two distinct ASD subtypes, idiopathic and 16p11.2 deletion, have common reductions in neural precursor cell (NPC) neurite outgrowth and migration even though whole genome sequencing demonstrates no genetic overlap between the datasets. To identify signaling differences that may contribute to these developmental defects, an unbiased phospho-(p)-proteome screen was performed. Surprisingly, despite the genetic heterogeneity, hundreds of shared p-peptides were identified between autism subtypes including the mTOR pathway. mTOR signaling alterations were confirmed in all NPCs across both ASD subtypes and mTOR modulation rescued ASD phenotypes and reproduced autism NPC-associated phenotypes in control NPCs. Thus, our studies demonstrate that genetically distinct ASD subtypes have common defects in neurite outgrowth and migration which are driven by the shared pathogenic mechanism of mTOR signaling dysregulation.</p>
Data from: Hypoxia blunts angiogenic signaling and upregulates the antioxidant system in elephant seal endothelial cells
<p><strong><em>Background</em></strong></p> <p>Elephant seals exhibit extreme hypoxemic tolerance derived from repetitive hypoxia/reoxygenation episodes they experience during diving bouts. Real-time assessment of the molecular changes underlying protection against hypoxic injury in seals remains restricted by their at-sea inaccessibility. Hence, we developed a proliferative arterial endothelial cell culture model from elephant seals and used RNA-seq, functional assays, and confocal microscopy to assess the molecular response to prolonged hypoxia.</p> <p><strong><em>Results</em></strong></p> <p>Seal and human endothelial cells exposed to 1% O<sub>2</sub> for up to 6 h respond differently to acute and prolonged hypoxia. Seal cells decouple stabilization of the hypoxia-sensitive transcriptional regulator HIF-1α from angiogenic signaling. Rapid upregulation of genes involved in glutathione (GSH) metabolism supports the maintenance of GSH pools, and intracellular succinate increases in seal but not human cells. High maximal and spare respiratory capacity in seal cells after hypoxia exposure occurs in concert with increasing mitochondrial branch length and independent from major changes in extracellular acidification rate, suggesting that seal cells recover oxidative metabolism without significant glycolytic dependency after hypoxia exposure.</p> <p><strong><em>Conclusions</em></strong></p> <p>We found that the glutathione antioxidant system is upregulated in seal cells during hypoxia, while this system remains static in comparable human cells. Furthermore, we found that in contrast to human cells, hypoxia exposure rapidly activates HIF-1 in seal cells, but this response is decoupled from the canonical HIF-angiogenesis pathway. These results highlight the unique mechanisms that confer extraordinary tolerance to limited oxygen availability in a champion diving mammal.</p>
Cell type specificity of glucocorticoid signaling in the adult mouse hippocampus
<p>The present study is based on the 10X scRNA-seq dataset published by the Allen Institute for Brain Science and publicly available at: <a href="https://portal.brain-map.org/atlases-and-data/RNA-seq/mouse-whole-cortex-and-hippocampus-10x">https://portal.brain-map.org/atlases-and-data/RNA-seq/mouse-whole-cortex-and-hippocampus-10x</a>. The cells from the hippocampus region were selected from the gene count expression matrix and pre-processed in R v3.6.1 according to the Seurat v3.1.5 standard pre-processing workflow for quality control, normalization, and analysis of scRNA-seq data. Here we make the final seurat object and other datasets further used in the code (<a href="https://github.com/eviho/10XHip2021_VihoEMG">https://github.com/eviho/10XHip2021_VihoEMG</a>) available for download. </p>
Chloroplast redox state changes indicate cell-to-cell signalling during the hypersensitive response
<p>We performed detailed spatiotemporal analysis of chloroplast redox response to potato virus Y (PVY) infection in resistant <em>Ny</em><em>‐</em><em>1</em>-gene-bearing potato and its transgenic counterpart with impaired SA accumulation and compromised resistance. We found that the chloroplasts are highly oxidized in the cells adjacent to the cell death zone at different stages after virus inoculation in both genotypes. This hypothesis is further supported by highly induced formation of stroma filled tubules that extend from chloroplasts (stromules) in the cells adjacent to signalling cells. This dataset s a deposit of all the raw microscopy images of the study, plus the relevant metadata in ISA-tab compliant folder structure. </p> <p>After receiving reviews, we have made an additional experiment using a ROS inhibitor. The raw and processed data for this is in a separate file: _S_chlROS_inhibitor.zip</p> <p><br> <br> </p> <p><strong>Additional information about the microscopy images in this data deposit </strong></p> <ol> <li>Images of which name ends with <strong>ch00/ch01/ch02</strong> are maximum projections from Z-stacks for each ROI for each of three channels: chlorophyll fluorescence (ch00), GFP fluorescence after excitation with 405 nm laser line (ch01) and GFP fluorescence after excitation with 488 laser line (ch02), exported from Leica LAS X software.</li> <li>Only mesophyll cells are included in z-stack, except for the experiments with GFP-tagged PVY where additional z-stacks including both mesophyll and epidermal cells were produced ( »_2« added in the image name, see images with the comment »epidermal cells included in z-stack« in S_PhenodataRedox).</li> <li>Images of which name ends with <strong>ch00.tif</strong> and <strong>ch00.tif_ratio</strong> are analysed images, obtained using in-house Matlab script. These images were obtained by the analysis of ch00/ch01/ch02 images with the following steps: conversion to grayscale, filtering out pixels of low intensity, conversion to binary format using spatial adaptive thresholding, a round or erosion and dilation to remove single pixel noise around the chloroplasts, followed by size-based segmentation of individual chloroplasts. The ratios of fluorescence intensities 405/488 were then calculated for each pixel belonging to the chloroplast masks obtained in the previous step. Results were calculated per image (normalized to the fraction of pixels belonging to chloroplasts) and per individual chloroplast in each image.</li> <li>In the experiments with GFP-tagged PVY, due to high background signal in the cell death zone as a result of virus derived GFP fluorescence, signal in the 488 channel and 405/488 ratio (images named »scaled 488« and »405/488 in chloroplasts« in ch00.tif_ratio) in the cell death zone are not accurate.</li> <li>Figures of which name ends with <strong>ch00.tif_spatial_ROI1/ROI2</strong> show the 405/488 ratios in ROI1 or ROI2, determined for each pixel inside chloroplast masks for each Bin. See Image analysis in Methods for details.</li> <li>Experiment names and image names correspond to the names in S_PhenodataRedox. Details regarding experimental set-up and transgenic lines used are specified in S_PhenodataRedox.</li> </ol> <p>The Zenodo_reanalysis.zip file contains processed microscopic images in a new red/blue colormap. </p>
Sclerostin blockade inhibits bone resorption through PDGF receptor signaling in osteoblast lineage cells
<p>While sclerostin-neutralizing antibodies (Scl-Ab) transiently stimulate bone formation by activating Wnt signaling in osteoblast lineage cells, they exert sustained inhibition of bone resorption, suggesting an alternate signaling pathway by which Scl-Ab control osteoclast activity. Since sclerostin can activate platelet-derived growth factor receptors (PDGFRs) in osteoblast lineage cells in vitro and PDGFR signaling in these cells induces bone resorption through M-CSF secretion, we hypothesized that the prolonged anti-catabolic effect of Scl-Ab could result from PDGFR inhibition. We show here that inhibition of PDGFR signaling in osteoblast lineage cells is sufficient and necessary to mediate prolonged Scl-Ab effect on M-CSF secretion and osteoclast activity in mice. Indeed, sclerostin co-activates PDGFRs independently of Wnt/β-catenin signaling inhibition, by forming a ternary complex with LRP6 and PDGFRs in pre-osteoblasts. In turn, Scl-Ab prevents sclerostin-mediated co-activation of PDGFR signaling and consequent M-CSF up-regulation in pre-osteoblast cultures, thereby inhibiting osteoclast activity in pre-osteoblast/osteoclast co-culture assays. These results provide a new potential mechanism explaining the dissociation between anabolic and anti-resorptive effects of long-term Scl-Ab.</p>
Cell migration with ERK signalling
<p>Movie following cells expressing ERK and a nuclei staining, tracked with TrackMate and later analyzed with MATLAB.</p> <p>See https://imagej.net/plugins/trackmate/trackmate-stardist for more details.</p> <p> </p>
Dataset related to: Empagliflozin protects glomerular endothelial cell architecture in experimental diabetes through the VEGF-A/caveolin-1/PV-1 signaling pathway
<p>The files contain all the dataset included in the manuscript divided by figures.</p> <p>Abstract<br> In addition to having blood glucose-lowering effects, inhibitors of sodium glucose cotransporter 2 (SGLT2) afford renoprotection in diabetes. We sought to investigate which components of the glomerular filtration barrier could be involved in the antiproteinuric and renoprotective effects of SGLT2 inhibition in diabetes. BTBR (black and tan, brachyuric) <em>ob/ob</em> mice that develop a type 2 diabetic nephropathy received a standard diet with or without empagliflozin for 10 weeks, starting at 8 weeks of age, when animals had developed albuminuria. Empagliflozin caused marked decreases in blood glucose levels and albuminuria but did not correct glomerular hyperfiltration. The protective effect of empagliflozin against albuminuria was not due to a reduction in podocyte damage as empagliflozin did not affect the larger podocyte filtration slit pore size nor the defective expression of nephrin and nestin. Empagliflozin<br> did not reduce the thickening of the glomerular basement membrane. In BTBR <em>ob/ob</em> mice, the most profound abnormality seen using electron microscopy was in the endothelial aspect of the glomerular capillary, with significant loss of endothelial fenestrations. Remarkably, empagliflozin ameliorated the subverted microvascular endothelial ultrastructure. Caveolae and bridging diaphragms between adjacent endothelial fenestrae were seen in diabetic mice and associated with increased expression of caveolin-1 and the appearance of PV-1. These endothelial abnormalities were limited by the SGLT2 inhibitor. Although no expression of SGLT2 was found in glomerular endothelial cells, SGLT2 was expressed in the podocytes of diabetic mice. VEGF-A, which is a known stimulus for endothelial caveolin-1 and PV-1, was increased in podocytes of BTBR <em>ob/ob</em> mice and normalized by SGLT2 inhibitor treatment.<br> Thus, empagliflozin’s protective effect on the glomerular endothelium of diabetic mice could be due to a limitation of the paracrine signaling of podocyte-derived VEGF-A that resulted in a reduction of the abnormal endothelial caveolin-1 and PV-1, with the consequent preservation of glomerular endothelial function and permeability.</p>
Oncogenic signalling is coupled to colorectal cancer cell differentiation state
<p>Mass cytometry and single-cell RNA-sequencing data as well as R Markdown reports to reproduce the figures of our publication.</p> <p>Raw MC data were saved post de-convolution, spillover-compensation, and removal of calibration bead events. Gates for singlets and non-dead cells (low_Pt) are included as logical columns and should be applied prior to usage.</p> <p>As we performed random sampling to equalise cell numbers across conditions, batch normalisation, and used non-linear dimensionality reduction techniques (UMAP and Diffusion Maps), resulting plots may differ slightly from the published figures, yet still support the drawn conclusions. Already normalised and/or sampled data as well as pre-computed UMAP and Diffusion Map coordinates are included in this data set to reproduce the manuscript figures exactly, as shown in the included report “figures_only”. For all details on the batch normalisation and data analysis steps performed, please consult the report “data_analysis” instead.</p>
Progesterone signaling in oviductal epithelial cells modulates the immune response to support preimplantation embryonic development
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Data for: Dysregulation of mTOR signaling mediates common neurite and migration defects in both idiopathic and 16p11.2 deletion autism neural precursor cells
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Data from: Hypoxia blunts angiogenic signaling and upregulates the antioxidant system in elephant seal endothelial cells
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Modeling single-cell heterogeneity in signaling dynamics of macrophages reveals principles of information transmission
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Data from: The brassinosteroid receptor gene BRI1 safeguards cell-autonomous brassinosteroid signaling across tissues
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Dysregulation in mTOR/HIF-1 signaling identified by proteo-transcriptomics of SARS- CoV-2 infected cells - Proteomic data obtained with Huh-7 cells
<p>Cultured human Huh-7 cells were infected with SARS-CoV-2 and harvested after 24, 48 and 72 h. The extracted proteins were processed in triplicates preparing for mass spectrometric analysis. Data acquisition was completed, including control samples of non-infected cells, following isobaric tandem mass tag (TMT) chemical labeling and on-line fractionation of the 12 combined biological replicates. The resulted vendor specific raw files (Thermo Scientific) of 12 fractions are provided.</p> <p>The data is further analyzed in order to identify regulated proteins upon SARS-CoV-2 infection to understand the underlying biological processes through pathway analysis. Additional details about the study is going to be completed in the manuscript already submitted for publication.</p>
Supplemental information for: Inhibition of CSF1R and KIT with pexidartinib reduces inflammatory signaling and cell viability in endometriosis
<p>Endometriosis is a common and debilitating disease, affecting ~170 million women worldwide. Affected patients have limited therapeutic options such as hormonal suppression or surgical excision of the lesions, though therapies are often not completely curative. Targeting receptor tyrosine-kinases (RTKs) could provide a nonhormonal treatment option for endometriosis. We determined that two RTKs, Macrophage colony stimulating factor receptor (CSF1R) and Mast/stem cell growth factor receptor KIT (KIT), are overexpressed in endometriotic lesions and could be novel nonhormonal therapeutic targets for endometriosis. The kinase activity of CSF1R and KIT is suppressed by pexidartinib, a small molecule inhibitor that was recently approved by the US Food and Drug Administration (FDA). Using immunohistochemistry, we detected CSF1R and KIT in endometriotic tissues obtained from peritoneal lesions, colorectal lesions, and endometriomas. Specifically, we show that KIT is localized to the epithelium of the lesions, while CSF1R is expressed in the stroma and macrophages of the endometriotic lesions. Given the high epithelial expression of CSF1R and KIT, 12Z endometriotic epithelial cells were used to evaluate the efficacy of dual CSF1R and KIT inhibition with pexidartinib. We found that pexidartinib suppressed activation in 12Z cells of JNK, STAT3 and AKT signaling pathways, which control key pro-inflammatory and survival networks within the cell. Using quantitative real time PCR, we determined that pexidartinib suppressed interleukin 8 (<em>IL8) </em>and cyclin D1 (<em>CCND1) </em>expression<em>.</em> Lastly, we demonstrated that pexidartinib decreased cell growth and viability.<em> </em>Overall, these results indicate that pexidartinib-mediated CSF1R and KIT inhibition reduces pro-inflammatory signaling and cell viability in endometriosis.</p>
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.