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2,167 results for “Interferons”
Transcriptome analysis of the effect of over-expressing H2A.J mutants in proliferating WI38 fibroblasts for the paper entitled: The H2A.J histone variant contributes to Interferon-Stimulated Gene expression in senescence by its weak interaction with H1 and the derepression of repeated DNA sequences
<p>Abstract for overall study:</p> <p>The histone variant H2A.J was previously shown to accumulate in senescent human fibroblasts with persistent DNA damage to promote inflammatory gene expression, but its mechanism of action was unknown. We show that H2A.J accumulation contributes to weakening the association of histone H1 to chromatin and increasing its turnover. Decreased H1 in senescence is correlated with increased expression of some repeated DNA sequences, increased expression of STAT/IRF transcription factors, and transcriptional activation of Interferon-Stimulated Genes (ISGs). The H2A.J-specific Val-11 moderates the transcriptional activity of H2A.J, and H2A.J-specific Ser-123 can be phosphorylated in response to DNA damage with potentiation of its transcriptional activity by the phospho-mimetic S123E mutation. Our work demonstrates the functional importance of H2A.J-specific residues and potential mechanisms for its function in promoting inflammatory gene expression in senescence.</p> <p>Specific description for this dataset:</p> <p>H2A.J differs from canonical H2A only by a valine at position 11 instead of alanine, and the 7 C-terminal amino acids containing a potential minimal phosphorylation site SQ for DNA-damage response kinases. To test the functional importance of these H2A.J-specific sequences, we mutated Val-11 to Ala as is found in all canonical H2A sequences, and we mutated Ser-123 to either Glu to mimic a phospho-serine residue or to Ala to prevent phosphorylation. We also substituted the C-terminus of H2A.J with the C-terminus of H2A. These mutants, WT-H2A.J and canonical H2A-type1 were ectopically expressed in proliferating fibroblasts, and their microarray transcriptomes were compared to that of proliferating and senescent fibroblasts without ectopic histone expression. Genome-wide transcriptome analysis indicated that senescent fibroblasts clustered distinctly from proliferating fibroblasts, and proliferating fibroblasts expressing the H2A.J-V11A and H2A.J-S123E mutants clustered distinctly from fibroblasts expressing the other H2A.J mutants, WT-H2A.J, and H2A. Hallmark gene set enrichment analysis of the transcriptomes of fibroblasts expressing H2A.J-V11A or H2A.J-S123E versus control proliferating fibroblasts indicated that they showed the same highly significant enrichment for the Epithelial-Mesenchyme Transition, TNF-Alpha Signaling Via NF-kB, and Inflammatory Response gene sets. Notable inflammatory genes including IL1A, IL1B, IL6, CXCL8, and CCL2 are contained in these gene sets and are often induced in senescence as part of the senescence-associated secretory phenotype. Heat maps showed that the H2A.J-V11A and H2A.J-S123E mutants were particularly apt at activating the expression of these inflammatory genes in proliferating fibroblasts</p>
Type III interferons may suppress viral infections by triggering cell death -- Imaging Dataset
<p>This dataset accompanies the article "Type III interferons may suppress viral infections by triggering cell death". Earlier version is available as a preprint, <a href="https://doi.org/10.1101/2024.09.09.612051" target="_blank" rel="noopener">https://doi.org/10.1101/2024.09.09.612051</a>. The updated dataset includes quantifications for Figure 7C and Figure 7D.</p>
Dataset for the stimulator of interferon genes protein (STING1) antibody screening study
<p><strong>This antibody characterization dataset is related to the F1000 research article openly available at F1000Research.</strong></p> <p><em>This dataset contains the following underlying raw data for a study which characterized sixteen antibodies for the stimulator of interferon genes protein (STING1) in western blot, immunoprecipitation and immunofluorescence. The corresponding study is accessible on the YCharOS community on Zenodo (<a href="https://doi.org/10.5281/zenodo.11582350">https://doi.org/10.5281/zenodo.11582350</a>).</em></p> <p><em>The Dataset is in the format of a zip file. Once downloaded, please expand the zip file to access the folders containing the underlying data for Western blot (Wb), immunoprecipitation (IP) and immunofluorescence (IF).</em></p>
A novel phosphoproteomic landscape evoked in response to type I interferon in the brain and in glial cells
<p>Type I interferons (IFN-I) are key responders to central nervous system infection and injury. They mediate their effects primarily via transcriptional regulation of several hundred interferon-regulated genes. Using a mouse model for IFN-I-induced neurodegeneration, we identified widespread protein phosphorylation as a new mechanism by which IFN-I mediate their effects. Protein phosphorylation aligned with the clinical hallmarks and pathological outcome, including impaired development, motor dysfunction and seizures. <em>In vitro</em> experiments revealed extensive and rapid IFN-I-induced protein phosphorylation in microglia and astrocytes, the brain’s primary IFN-I-responding cells. Response to acute IFN-I stimulation was independent of gene expression and mediated by a small number of kinase families. The changes in the phosphoproteome affected a diverse range of cellular processes and functional analysis suggested that this response induced an immediate reactive state and prepared cells for subsequent transcriptional responses. Our studies reveal a hitherto unappreciated role for changes in the protein phosphorylation landscape in cellular responses to IFN-I and thus provide insights for novel diagnostic and therapeutic strategies for neurological diseases caused by IFN-I.</p>
A novel phosphoproteomic landscape evoked in response to type I interferon in the brain and in glial cells
<p>Type I interferons (IFN-I) are key responders to central nervous system infection and injury. They mediate their effects primarily via transcriptional regulation of several hundred interferon-regulated genes. Using a mouse model for IFN-I-induced neurodegeneration, we identified widespread protein phosphorylation as a new mechanism by which IFN-I mediate their effects. Protein phosphorylation aligned with the clinical hallmarks and pathological outcome, including impaired development, motor dysfunction and seizures. <em>In vitro</em> experiments revealed extensive and rapid IFN-I-induced protein phosphorylation in microglia and astrocytes, the brain’s primary IFN-I-responding cells. Response to acute IFN-I stimulation was independent of gene expression and mediated by a small number of kinase families. The changes in the phosphoproteome affected a diverse range of cellular processes and functional analysis suggested that this response induced an immediate reactive state and prepared cells for subsequent transcriptional responses. Our studies reveal a hitherto unappreciated role for changes in the protein phosphorylation landscape in cellular responses to IFN-I and thus provide insights for novel diagnostic and therapeutic strategies for neurological diseases caused by IFN-I.</p>
Figure. Interferon alpha-A based phylogenetic tree (neighbor joining method) constructed by MEGA 6.1 for Punjab urial in comparison with other mammalian species sequences available from GenBank (NCBI). in Characterization of interferon alpha of major histocompatibility complex class I in Punjab urial (Ovis vignei punjabiensis)
Figure. Interferon alpha-A based phylogenetic tree (neighbor joining method) constructed by MEGA 6.1 for Punjab urial in comparison with other mammalian species sequences available from GenBank (NCBI).
Interferon-induced activation of dendritic cells and monocytes by yellow fever vaccination correlates with early antibody responses
<p>Bulk RNA-seq analysis of sorted subpopulations isolated from PBMC of yellow fever vaccinees from before and 3, 7, 14 and 28 days after vaccination and single cell RNA-seq analysis of sorted DC and monocytes fractions isolated from PBMC of of yellow fever vaccinees from before and 3 and 7 days after vaccination.</p>
Pegylated Interferon Lambda Treatment for COVID-19
ClinicalTrials.gov study NCT04343976. IPD Sharing: YES. Countries: 1. Publications: 1.
PEDS-C: Pegylated Interferon +/- Ribavirin for Children With Hepatitis C
ClinicalTrials.gov study NCT00100659. IPD Sharing: YES. Countries: 1. Publications: 9.
Data from: Major group-B enterovirus populations deleted in the noncoding 5' region of genomic RNA modulate activation of the type I interferon pathway in cardiomyocytes and induce myocarditis
<p>Major 5'-terminally deleted (5'TD) RNA forms of group-B coxsackievirus (CVB-5'TD) has been associated with myocarditis in both mice and humans. Although it is known that interferon-β (IFN-β) signaling is critical for an efficient innate immune response against CVB-induced myocarditis, the link between CVB-5'TD RNA forms and type I IFN signaling in cardiomyocytes remains to be explored. In a mouse model of CVB3/28-induced myocarditis, major early-emerging forms of CVB-5'TD RNA have been characterized as replicative viral populations that impair IFN-β production in the heart. Synthetic CVB3/28 RNA forms mimicking each of these major 5'TD virus populations were transfected in mice and have been shown to modulate innate immune responses in the heart and to induce myocarditis in mice. Remarkably, transfection of synthetic viral RNA with deletions in the secondary structures of the 5'-terminal CVB3 RNA domain I, modifying stem-loops "b", "c" or "d", were found to impair IFN-β production in human cardiomyocytes. In addition, the activation of innate immune response by Poly(I:C), was found to restore IFN-β production and to reduce the burden of CVB-5'TD RNA-forms in cardiac tissues, thereby reducing the mortality rate of infected mice. Overall, our results indicate that major early-emerging CVB3 populations deleted in the domain I of genomic RNA, in the 5' noncoding region, modulate the activation of the type I IFN pathway in cardiomyocytes and induce myocarditis in mice. These findings shed new light on the role of replicative CVB-5'TD RNA forms as key pathophysiological factors in CVB-induced human myocarditis.</p>
Crystal structure of olive flounder [Paralichthys olivaceus] interferon gamma at 2.3 Angstrom resolution - diffraction data
<p>Diffraction images, Bessy II (Berlin), MX 14.1, 12.5.2017, PDB ID 6F1E</p>
Chronic social defeat stress induces meningeal neutrophilia via type I interferon signaling: single cell RNA sequencing data
<p>Meningeal single cell RNA sequencing data</p> <p>Meningeal samples were collected from both dorsal and ventral skull, avoiding inclusion of choroid plexus. Samples were digested in 2.5 mg/mL Collagenase D (Cat. #11088858001; Roche) and 12.5 μL of 0.5 mg/mL DNAseI (Cat. #L5002139; Worthington), put on a shaker at 370C for 30 m, diluted with cold HBSS + 0.1% BSA, and mashed through a 70 μm cell strainer prior to sorting.</p> <p>Data represent live, nucleated, singlet cells (DAPI-DRAQ5+) sorted on a BD FACS Aria Fusion into HBSS + 10% FBS prior to droplet encapsulation using 10x Genomics’ Drop-seq platform (Chromium v2).</p> <p>10X chip lane is indicate by 'group' column</p> <p>Group 1 = 4 pooled homecage control (unstressed) mice</p> <p>Group 2 = 4 pooled homecage control (unstressed) mice</p> <p>Group 3 = 4 pooled mice exposed to chronic social defeat for 14 days; tissue was collected 2 hours following final defeat</p> <p>See the following repositories for data processing:</p> <p><a href="https://github.com/maryellenlynall/2019_bcell_stress/blob/master/bcellstress20.Rmd">https://github.com/maryellenlynall/2019_bcell_stress/</a> (processing from raw files starts at bcellstress020.Rmd)</p> <p><a href="https://github.com/staceykigar/meningeal_neut/">https://github.com/staceykigar/meningeal_neut/</a></p> <p>We also provide a processed dataset (processed.RData) with assays 'counts' and 'logcounts' which is the processed single cell object saved at line "# Save object for upload to Zenodo" in script <a href="https://github.com/staceykigar/meningeal_neut/">https://github.com/staceykigar/meningeal_neut/</a>neutrophilstress01.Rmd </p> <p>Cluster annotations are in sce$Annotation</p> <p>Neutrophil subcluster annotations are in sce$Subcluster</p> <p>Sample condition is in sce$cond, where "HC" indicates homecage control and "SD" indicates chronic social defeat</p> <p>10X chip lane is in sce$group</p>
Macrophage fumarate hydratase restrains mtRNA-mediated interferon production
<p>Metabolic rewiring underlies macrophage effector functions, but the mechanisms involved remain incompletely defined. Here, using unbiased metabolomics and stable isotope-assisted tracing, we show induction of an inflammatory aspartate-argininosuccinate shunt following LPS stimulation. The shunt, supported by increased ASS1 expression, also leads to increased cytosolic fumarate levels and fumarate-mediated protein succination. Pharmacologic inhibition and genetic ablation of the TCA cycle enzyme FH further elevates intracellular fumarate levels, suppresses mitochondrial respiration, and increases mitochondrial membrane potential. RNA sequencing and proteomic analysis demonstrate profound inflammatory effects resulting from FH inhibition. Of note, acute FH inhibition suppresses IL-10 expression leading to increased TNF-α secretion, an effect recapitulated by fumarate esters. Unexpectedly, FH inhibition, but not fumarate esters, also increases IFN-β production through mechanisms that are driven by mitochondrial RNA (mtRNA) release and activation of the RNA sensors TLR7 and RIG-I/MDA5. This effect is recapitulated endogenously when FH is suppressed following prolonged LPS stimulation. Furthermore, cells from SLE patients also exhibit FH suppression, indicating a potential pathogenic role for this process in human disease. We therefore identify a protective role for FH in maintaining appropriate macrophage cytokine and interferon responses.</p> <p>Data from this study that is included in this Dryad submission is as follows:</p> <p>1. RNA sequencing of non-stimulated (with vehicle DMSO) or lipopolysaccaharide-stimulated (4 h) murine bone marrow-derived macrophages (BMDMs) pre-treated with vehicle (DMSO), 20 micromolar fumarate hydratase inhibitor 1 (FHIN1) or 25 micromolar dimethylfumarate (DMF) for 3 h. Three biological replicates per condition.</p> <p>2. Label-free proteomics of lipopolysaccaharide-stimulated (4 h) murine bone marrow-derived macrophages (BMDMs) pre-treated with vehicle (DMSO), 20 micromolar fumarate hydratase inhibitor 1 (FHIN1) or 25 micromolar dimethylfumarate (DMF) for 3 h. Five biological replicates per condition. </p> <p>3. Metabolomics source data used for the study.</p>
Sofosbuvir With Pegylated Interferon and Ribavirin Hepatitis C Virus (HCV) Genotypes 1,4,5,6
ClinicalTrials.gov study NCT01329978. IPD Sharing: Not stated. Countries: 2. Publications: 2.
A Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Antiviral Activity of Multiple Doses of ABT-333 Alone and in Combination With Pegylated Interferon (pegIFN) and Ribavirin (RBV) in S
ClinicalTrials.gov study NCT00851890. IPD Sharing: Not stated. Countries: 2. Publications: 1.
A Multicentre Study of the Efficacy and Safety of Supplementary Treatment With Cholecalciferol in Patients With Relapsing Multiple Sclerosis Treated With Subcutaneous Interferon Beta-1a 44 µg 3 Times
ClinicalTrials.gov study NCT01198132. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Study to Evaluate Pegylated Interferon Lambda Monotherapy in Patients With Chronic Hepatitis Delta Virus Infection
ClinicalTrials.gov study NCT02765802. IPD Sharing: Not stated. Countries: 3. Publications: 3.
Intraperitoneal Infusion of Autologous Monocytes With Sylatron (Peginterferon Alfa-2b) and Actimmune (Interferon Gamma-1b) in Women With Recurrent or Refractory Ovarian Cancer, Fallopian Tube Cancer o
ClinicalTrials.gov study NCT02948426. IPD Sharing: YES. Countries: 1. Publications: 6.
Efficacy and Safety of BI 201335 (Faldaprevir) in Combination With Pegylated Interferon-alpha and Ribavirin in Treatment-naïve Genotype 1 Hepatitis C Infected Patients (STARTverso 1)
ClinicalTrials.gov study NCT01343888. IPD Sharing: Not stated. Countries: 11. Publications: 3.
Efficacy and Safety of BIIB019 (Daclizumab High Yield Process) Versus Interferon β 1a in Participants With Relapsing-Remitting Multiple Sclerosis
ClinicalTrials.gov study NCT01064401. IPD Sharing: Not stated. Countries: 28. Publications: 7.
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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)
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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.