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2,678 results for “cell signalling”
Integrated plasma proteomic and single-cell immune signaling network signatures demarcate mild, moderate, and severe COVID-19
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Identification of signaling networks associated with lactate modulation of macrophages and dendritic cells
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Data from: Sex-specific thermoregulatory effects of estrogen signaling in <em>Reprimo</em> lineage cells
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Data from: Gastrointestinal gd T cells reveal upregulated T-cell transcripts and signaling pathways during peanut oral immunotherapy
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Data from: Ca²⁺ signaling in myenteric interstitial cells of Cajal (ICC-MY) and their role as conditional pacemakers in the colon
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Supplementary data for: Ligand-specific tuning of CLEC10A signalling strength and dendritic cell responses through engagement of different GalNAc-containing glycan structures
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Soluble T-cadherin promotes pancreatic β-cell proliferation by upregulating Notch signaling
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Data from: Conditional requirement for dimerization of the membrane-binding module for BTK signaling in lymphocyte cell lines
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Data from: Prolonged cell cycle arrest in response to DNA damage in yeast requires the maintenance of DNA damage signaling and the spindle assembly checkpoint
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Numeric data from: Non-autonomous insulin signaling delays mitotic progression in C. elegans germline stem and progenitor cells
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Sphingosine-1-phosphate signaling regulates the ability of Müller glia to become neurogenic, proliferating progenitor-like cells
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Data from: Allospecific splenic Tr1 cells drive effector T cell exhaustion through upregulated Areg-EGFR signaling to promote transplant tolerance
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Data from: Diethylcarbamazine elicits calcium signals in HEK293 cells by activation of heterologously expressed <em>Brugia malayi</em> TRP-2b channels
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Neuronal octopamine signaling regulates mating-induced germline stem cell increase in female Drosophila melanogaster
<p>Stem cells fuel the development and maintenance of tissues. Many studies have addressed how local signals from neighboring niche cells regulate stem cell identity and their proliferative potential. However, the regulation of stem cells by tissue-extrinsic signals in response to environmental cues remains poorly understood. Here we report that efferent octopaminergic neurons projecting to the ovary are essential for germline stem cell (GSC) increase in response to mating in female <i>Drosophila</i>. The neuronal activity of the octopaminergic neurons is required for mating-induced GSC increase as they relay the mating signal from Sex peptide receptor-positive cholinergic neurons. Octopamine and its receptor Oamb are also required for mating-induced GSC increase via intracellular Ca<sup>2+</sup> signaling. Moreover, we identified Matrix metalloproteinase-2 as a downstream component of the octopamine-Ca<sup>2+</sup> signaling to induce GSC increase. Our study provides a mechanism describing how neuronal system couples stem cell behavior to environmental cues through stem cell niche signaling.</p>
Endocannabinoid signalling in stem cells and cerebral organoids drives differentiation to deep layer projection neurons via CB1 receptors
<p>The endocannabinoid (eCB) system, <i>via</i> cannabinoid CB<sub>1</sub> receptor, regulates neurodevelopment by controlling neural progenitor proliferation and neurogenesis. CB<sub>1</sub> receptor signalling <i>in vivo</i> drives corticofugal deep layer projection neuron development through the regulation of <span>BCL11B </span>and <span>Satb2</span> transcription factors. Here, we investigated the role of eCB signalling in mouse pluripotent embryonic stem cell-derived neuronal differentiation. Characterization of the eCB system revealed increased expression of eCB-metabolizing enzymes, eCB ligands and CB<sub>1</sub> receptors along neuronal differentiation. CB<sub>1</sub> receptor knockdown inhibited neuronal differentiation of deep layer neurons and increased upper layer neuron generation, and this phenotype was rescued by CB<sub>1</sub> re-expression. Pharmacological regulation with CB<sub>1</sub> receptor agonists or elevation of eCB tone with a monoacylglycerol lipase inhibitor promoted neuronal differentiation of deep layer neurons at the expense of upper layer neurons. Patch-clamp analyses revealed that enhancing cannabinoid signalling facilitated neuronal differentiation and functionality. Noteworthy, incubation with CB<sub>1</sub> receptor agonists during human iPSC-derived cerebral organoid formation also promoted the expansion of BCL11B<sup>+</sup> neurons. These findings unveil a cell-autonomous role of eCB signalling that, <i>via</i> CB<sub>1</sub> receptor, promotes mouse and human deep layer cortical neuron development.</p>
Data from: A proteomics approach for the identification of cullin-9 (CUL9) related signaling pathways in induced pluripotent stem cell models
<p>CUL9 is a non-canonical and poorly characterized member of the largest family of E3 ubiquitin ligases known as the Cullin RING ligases (CRLs). Most CRLs play a critical role in developmental processes, however, the role of CUL9 in neuronal development remains elusive. We determined that deletion or depletion of CUL9 protein causes aberrant formation of neural rosettes, an in vitro model of early neuralization. In this study, we applied mass spectrometric approaches in human pluripotent stem cells (hPSCs) and neural progenitor cells (hNPCs) to identify CUL9 related signaling pathways that may contribute to this phenotype. Through LC-MS/MS analysis of immunoprecipitated endogenous CUL9, we identified several subunits of the APC/C, a major cell cycle regulator, as potential CUL9 interacting proteins. Knockdown of the APC/C adapter protein FZR1 resulted in a significant increase in CUL9 protein levels, however, CUL9 does not appear to affect protein abundance of APC/C subunits and adapters or alter cell cycle progression. Quantitative proteomic analysis of CUL9 KO hPSCs and hNPCs identified protein networks related to metabolic, ubiquitin degradation, and transcriptional regulation pathways that are disrupted by CUL9 deletion in both hPSCs and hNPCs. The results of our study build on current evidence that CUL9 may have unique functions in different cell types potentially contributing to the difficulty of identifying CUL9 substrates.</p> <p><strong>Information on data/files</strong>:</p> <p><em>Please first unzip Figure_4_CUL9-IP-LCMSMS-data.zip and Figure_7_iTRAQ-data.zip, then follow the description below.</em></p> <p>CUL9 immunoprecipitation from whole lysates collected for hPSCs were analyzed using LC/MS-MS. IgG was used as a control to determine proteins specifically enriched in the CUL9 IP. This data correlates to Figure 4 of the associated manuscript.</p> <p>Initial CUL9 immunoprecipitation was performed by VG and analyzed by LC-MS/MS at UNC.</p> <p>Fig4-LCMSMS_IPCUL9_Replicate1_UNC</p> <p>Two more immunoprecipitations were performed by VG and analyzed by LC-MS/MS at Vanderbilt University MSRC Proteomics Core. The first run (replicate 1) was used to produce the STRING figure in the associated manuscript, as well as the volcano plot in Supplemental Figure 8.</p> <p>Two Scaffold files contain raw data and our analysis parameters:</p> <ul> <li>Fig4-LCMSMS_IPCUL9_Replicate2_Vanderbilt</li> <li>Fig4-LCMSMS_LCMSMS_IPCUL9_Replicate3_Vanderbilt</li> </ul> <p>Excel files exported from the above Scaffold files contain the raw data in excel format including spectral counts, peptide counts, protein probability, and detailed raw data as it pertains to each identified protein. See these data sets in the folders below:</p> <ul> <li>Fig4-LCMSMS_IPCUL9_Run2_Vanderbilt_CompleteDataSet</li> <li>Fig4-LCMSMS_IPCUL9_Run3_Vanderbilt_CompleteDataSet</li> </ul> <p>CUL9 KO clones were used to identify proteins increased or decreased compared to parental wild-type cell lines using iTRAQ. This data correlates to Figure 8 of the associated manuscript. Two iTRAQ experiments were performed to identify proteins altered in CUL9 KO iPSCs, neural stem cells (NSCs), and NPCs. Each set of experiments was duplicated – each in a different isogenic CUL9 KO clone (Clone 20 or Clone B)</p> <p><strong>iTRAQ labeling of experiment one is as follows:</strong></p> <ol> <li>Label 115: Parental WT NSCs</li> <li>Label 117: CUL9 KO Clone 20 or B NSCs</li> <li>Label 114: Parental WT NPCs</li> <li>Label 116: CUL9 KO Clone 20 or B NPCs</li> </ol> <p>Files containing raw and analyzed data of experiment one are labeled as follows:</p> <ul> <li>Fig7_Experiment1_Clone 002_compared-to-NSC-WT</li> <li>Fig7_Experiment1_Clone001-compared-to-NSC-WT</li> <li>Fig7_Experiment1_Clone001iPSC_compared-to-iPSCWT</li> <li>Fig7_Experiment1_Clone002_compared-to-iPSCWT</li> </ul> <p><strong>iTRAQ labeling of experiment two is as follows:</strong></p> <p>For Clone 20:</p> <ol> <li>Label 115: Parental WT NSCs</li> <li>Label 117: CUL9 KO Clone 20 or B NSCs</li> <li>Label 114: Parental WT iPSCs</li> <li>Label 116: CUL9 KO Clone 20 or B iPSCs</li> </ol> <p>Files containing raw and analyzed data of experiment two are labeled as follows:</p> <ul> <li>Fig7_Experiment2_Clone001NPC_Compared-to-NPC-WT</li> <li>Fig7_Experiment2_Clone001NPC_Compared-to-NSC-WT</li> <li>Fig7_Experiment2_Clone002NPC_Compared-to-NPC-WT</li> <li>Fig7_Experiment2_Clone002NPC_Compared-to-NSC-WT</li> </ul> <p>Please note that the first tab of each excel document contains the full raw data set before analysis. All other tabs contain analyzed data comparing the proteins identified in two cell lines. Analyzed tabs are labeled to indicate which cell lines are being compared. Please note that the CUL9 isogenic clones Clone 20=Clone#1 and Clone B=Clone#2 as referenced in the associated manuscript.</p> <p>Detailed information about the protocols used for collection and analysis of this data can be found in the supplemental information within the associated manuscript.</p>
Data from: Early mechanistic events induced by low molecular weight polycyclic aromatic hydrocarbons in mouse lung epithelial cells: a role for eicosanoid signaling
Low molecular weight polycyclic aromatic hydrocarbons (LMW PAHs; <206.3 g/mol) are under regulated environmental contaminants (e.g., secondhand smoke) that lead to gap junction dysregulation, p38 MAPK activation, and increased mRNA production of inflammatory mediators, such as cytokines and cyclooxygenase (COX2), in lung epithelial cells. However, the early mechanisms involving lipid signaling through the arachidonic acid pathway and subsequent eicosanoid production leading to these downstream events are not known. Common human exposures are to mixtures of LMW PAH's, thus C10 cells (a mouse lung epithelial cell line) were exposed to a representative binary PAH mixture, 1-methylanthracene (1-MeA) and fluoranthene (Flthn), for 30 min – 24 h with and without p38 and cytosolic phospholipase A2 (cPLA2) inhibitors. cPLA2 inhibition reversed PAH-induced phospho-p38 MAPK activation and gap junction dysregulation at 30 min. A significant biphasic increase of cPLA2 protein was observed at 30 min, 2, & 4 h, as well as COX2 protein at 2 & 8 h. Untargeted metabolomics demonstrated a similar trend with significantly changing metabolites at 30 min & 4 h of exposure relative to 1 h; a "cPLA2-like" subset of metabolites within the biphasic response were predominately phospholipids. argeted metabolomics showed several eicosanoids (e.g., prostaglandin D2 (PGD2), PGE2α) were significantly increased at 4, 8, and 12 h following exposure to the binary PAH mixture and this effect was p38-dependent. Lastly, PAH metabolism was not observed until after 8 h. These results indicate an early lipid signaling mechanism of PAH toxicity in lung epithelial cells due to parent PAH compounds.
A single-cell atlas of Drosophila trachea reveals glycosylation-mediated Notch signaling in cell fate specification
<p>Processed data files for the following article:</p><p>Li Y, Lu T, Dong P, Chen J, Zhao Q, Wang Y, Xiao T, Wu H, Zhao Q and Huang H. A single-cell atlas of Drosophila trachea reveals glycosylation-mediated Notch signaling in cell fate specification.</p><p>Please also refer to code at https://github.com/Tianfeng-Lu/single-cell-atlas-of-fly-trachea</p>
Scripts reproducing the analyses of the paper "HCMV exploits STING signaling and counteracts IFN and ISG induction to facilitate infection of dendritic cells" by Costa et al
<p>This is the code to reproduce the data analyses in the manuscript "HCMV exploits STING signaling and counteracts IFN and ISG induction to facilitate infection of dendritic cells".</p> <p>Required software and packages:</p> <p>R (4.2.1)<br>circlize (0.4.15)<br>ComplexHeatmap (2.12.1)<br>cowplot (1.1.1)<br>future (1.28.0)<br>ggalluvial (0.12.5)<br>ggpubr (0.4.0)<br>ggrepel (0.9.1)<br>GSVA (1.44.5)<br>msigdbr (7.5.1)<br>patchwork (1.1.2)<br>plyr (1.8.7)<br>presto (1.0.0)<br>RColorBrewer (1.1-3)<br>reshape2 (1.4.4)<br>sctransform (0.3.5)<br>Seurat (4.2.0)<br>SeuratDisk (0.0.0.9020)<br>SeuratWrappers (0.3.1)<br>velocyto.R (0.6)</p> <p>Howto: Execute all scripts in order by first changing into the directory, and then executing the script:</p> <pre><code>cd 00_QC; Rscript 00_QC.R; cd ..</code></pre>
Raw data of the publication ''Radical' differences between two FLIM microscopes affect interpretation of cell signaling dynamics'
<p>Raw data and data used to create the figures.</p>
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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.