Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
2,648
datasets available to search
ShareScore release 0.9.0
Dataset results
2,648 results for “MIR”
Integrin restriction by miR-34 protects germline progenitors from cell death during aging
Open the record for dataset details and reuse information.
Circulating myeloid-derived suppressor cells facilitate invasion of thyroid cancer cells by repressing miR-486-3p
<p>Background: Myeloid-derived suppressor cells (MDSCs) have become increasingly recognized as facilitators of tumor development. However, the role of MDSCs in papillary thyroid carcinoma (PTC) progression has not been clearly explored.</p> <p>Objective: We aimed to evaluate the levels and function of circulating MDSCs in PTC.</p> <p>Methods: The proportion of circulating polymorphonuclear (PMN)-MDSCs and mononuclearMDSCs from patients with PTC or benign thyroid nodules and healthy controls was measured using flow cytometry. For immunosuppressive activity analysis, sorted circulating MDSCs were cocultured with CD3/CD28-costimulated T lymphocytes and the proliferation of T cells was determined. PTC cell lines (TPC-1 and BC-PAP) were cocultured with PMN-MDSCs, and the effects on cell migration, invasion, proliferation, and apoptosis were evaluated. The differential expressed microribonucleic acids (RNAs) and messenger RNAs and their function were also explored in TPC-1 cells cocultured with or without PMN-MDSCs.</p> <p>Results: PMN-MDSCs were increased in peripheral blood mononuclear cells of patients with PTC. Circulating PMN-MDSCs displayed strong T cell suppressive activity. PTC cells demonstrated enhanced invasive capabilities in vitro and in vivo when cocultured with sorted PMN-MDSCs. PMN-MDSCs decreased expression of miR-486-3p and activated nuclear factor kappa B2 (NF-κB2), a direct target of miR-486-3p. Rescue of miR-486-3p diminished the cell migration and invasion induced by PMN-MDSCs.</p> <p>Conclusion: Collectively, our work indicates that circulating PMN-MDSCs promote PTC progression. By suppressing miR-486-3p, PMN-MDSCs promote the activity of the NF-κB2 signaling pathway, resulting in accelerated invasion of PTC cells, which may provide new therapeutic strategies for treatment of thyroid cancer. </p>
Data from: Despite high levels of expression in thymic epithelial cells, miR-181a1 and miR-181b1 are not required for thymic development
MicroRNAs (miRNAs) have been shown to be key modulators of post-transcriptional gene silencing in many cellular processes. In previous studies designed to understand the role of miRNAs in thymic development, we globally deleted miRNA exclusively in thymic epithelial cells (TECs), which are critical in thymic selection. This resulted in the loss of stromal cells that instruct T cell lineage commitment and affect thymocyte positive selection, required for mature T cell development. Since murine miR-181 is expressed in the thymus and miR-181 deficiency disrupts thymocyte development, we first quantified and thereby demonstrated that miR181a1 and miR181b1 are expressed in purified TECs. By generating mice with TEC targeted loss of miR-181a1 and miR-181b1 expression, we observed that neither TEC cellularity nor thymocyte number nor differentiation was adversely affected. Thus, disrupted thymopoiesis in miR-181 deficient mice was not due to miR-181 loss of expression in TECs. Importantly, in mice with restricted TEC deficiency of miR-181a1 and miR-181b1, there were similar numbers of mature T cells in the periphery in regards to frequencies, differentiation, and function as compared to controls. Moreover miR-181a1 and miR-181b1 were not required for maintenance of thymus integrity over time, as thymic involution was not accelerated in gene-targeted mice. Taken together our data indicate that miR-181a1 and miR-181b1 are dispensable for TEC differentiation, their control of thymocyte development and mature T cell export to and homeostasis within the periphery.
miR-1285-3p targets TPI1 to regulate the glycolysis metabolism signaling pathway of Tibetan sheep Sertoli cells
<p><span>Glycolysis in sertoli cells (SCs) can provide energy substrates for the development of spermatogenic cells. Triose phosphate isomerase 1 (TPI1) is one of the key catalytic enzymes involved in glycolysis. However, the biological function of TPI1 in SCs and its role in glycolytic metabolic pathways are poorly understood. On the basis of previous research, we isolated primary SCs from Tibetan sheep and overexpressed <em>TPI1</em> gene to determine its effect on the proliferation, glycolysis, and apoptosis of SCs. Secondly, we investigated the relationship between <em>TPI1</em> and miR-1285-3p, and whether miR-1285-3p regulates the proliferation and apoptosis of SCs, and participates in glycolysis by targeting <em>TPI1</em>. Results showed that overexpression of <em>TPI1</em> increased the proliferation rate and decreased apoptosis of SCs. In addition, overexpression of <em>TPI1</em> altered glycolysis and metabolism signaling pathways and significantly increased the amount of the final product lactic acid. Further analysis showed that miR-1285-3p inhibited <em>TPI1</em> by directly targeting its 3'untranslated region. Overexpression of miR-1285-3p suppressed the proliferation of SCs, and this effect was partially reversed by restoration of <em>TPI1</em> expression. In summary, this study shows that the miR-1285-3p/TPI1 axis regulates glycolysis in SCs. These findings add to our understanding of the regulation of spermatogenesis in sheep and other mammals.</span></p>
Data from: A short peptide exerts neuroprotective effects on cerebral ischemia-reperfusion injury by reducing inflammation via the miR-6328/IKKβ/NF-κB axis
<p><strong><span>Background</span></strong></p> <p><span>Despite considerable efforts, ischemic stroke (IS) remains a challenging clinical problem. Therefore, the discovery of effective therapeutic and targeted drugs based on the underlying molecular mechanism is crucial for effective IS treatment.</span></p> <p><strong><span>Methods</span></strong></p> <p><span>A cDNA-encoding peptide was extracted and identified from RNA extracted from <em>Rana limnocharis</em> skin, and its neuroprotective properties were evaluated using a middle cerebral artery occlusion/reperfusion (MCAO/R) model in rats and an oxygen-glucose deprivation/reperfusion (OGD/R) model in neuron-like PC12 cells. The underlying molecular mechanisms were explored using microRNA (miRNA) sequencing, quantitative real-time polymerase chain reaction</span><span>, dual-luciferase reporter gene assay, and western blotting.</span></p> <p><strong><span>Results</span></strong></p> <p><span>A new peptide (NP1) with an amino acid sequence of '</span><span>FLPAAICLVIKTC</span><span>' was identified. NP1 showed no obvious toxicities <em>in vivo</em> and <em>in vitro</em>. I</span><span>ntraperitoneal administration of NP1 (10 nmol/kg) effectively reduced the volume of cerebral infarction and relieved neurological dysfunction in MCAO/R model rats. Moreover, NP1 significantly alleviated the decrease in viability of PC12 cells induced by OGD/R. NP1 effectively suppressed inflammation by reducing interleukin-1β (</span><span>IL-1β) and </span><span>tumor necrosis factor-</span><span>α (</span><span>TNF-α) levels </span><em><span>in vitro</span></em><span> and <em>in vivo</em>. Furthermore, NP1 up-regulated the expression of miRNA-6328, which targeted down-regulation of the inflammation-related factor inhibitor kappa B kinase β (</span><span>IKKβ),</span><span> thereby reducing nuclear factor-kappa B p65</span><span> (NF-κB</span><span> p65) and inhibitor of </span><span>NF-κB</span><span> (I-</span><span>κ</span><span>B) phosphorylation and inhibiting the </span><span>NF-κB</span><span> pathway.</span></p> <p><strong><span>Conclusions</span></strong></p> <p><span>NP1 exerted neuroprotective effects by reducing inflammation via the miRNA-6328/IKKβ/NF-κB axis. This study highlights the importance of peptides in the development of new drugs, elucidation of </span><span>pathological mechanisms, and discovery of new drug targets.</span></p>
Mir castle
Мирский замок castle Mir Source: Objaverse 1.0 / Sketchfab
XDL_MIR_PAM_2024_Dataset
Open the record for dataset details and reuse information.
Data from: GATA2 controls lymphatic endothelial cell junctional integrity and lymphovenous valve morphogenesis through miR-126
Mutations in the transcription factor GATA2 cause lymphedema. GATA2 is necessary for the development of lymphatic valves (LVs) and lymphovenous valves (LVVs), and for the patterning of lymphatic vessels. Here, we report that GATA2 is not necessary for valvular endothelial cell (VEC) differentiation. Instead, GATA2 is required for VEC maintenance and morphogenesis. GATA2 is also necessary for the expression of cell junction molecules VE-Cadherin and Claudin5 in lymphatic vessels. We identified miR-126 as a target of GATA2, and miR-126-/- embryos recapitulate the phenotypes of mice lacking GATA2. Primary human lymphatic endothelial cells (HLECs) lacking GATA2 (GATA2ΔHLEC) have altered expression of Claudin5 and VE-Cadherin, and blocking miR-126 activity in HLECs phenocopies these changes in expression. Importantly, overexpression of miR-126 in GATA2ΔHLEC significantly rescues the cell junction defects. Thus, our work defines a new mechanism of GATA2 and uncovers miR-126 as a novel regulator of mammalian lymphatic vascular development.
Example micrographs of RNA polymerase II localization to the zebrafish microRNA miR-430 cluster
<p>Contains the raw images and MatLab scripts to show localization of recruited (Ser5P) and elongating (Ser2P) RNA polymerase II to the zebrafish microRNA miR-430 cluster. Embryos were fixed in the oblong stage of development, labeled by immunofluorescence, and images were recorded with an instant-SIM microscope.</p> <p>To produce example images, first run the extraction script, then the example images script. You need to add the bfmatlab importer function from OME for data import before running the extraction script. Otherwise, extracted data are also provided with this repository,</p>
The lncRNA TUG1 regulates Smac/DIABLO expression by competitively inhibiting miR-29b and modulates the apoptosis of lens epithelial cells in age-related cataracts
<p>As one of the first discovered lncRNAs, TUG1 has been reported to be widely expressed in a variety of tumours. It promotes cell proliferation, differentiation, apoptosis and migration. However, our understanding of its importance in cataracts is limited. This study aims to explore the mechanism by which TUG1 mediates the apoptosis of lens epithelial cells by regulating the miR-29b/Smac axis in age-related cataracts and to identify more strategies for the nonsurgical treatment of cataracts. In this experiment we found TUG1 and Smac were expressed at high levels in age-related cataract (ARC) samples and HLEB3 cells treated with H2O2, while miR-29b expression was decreased. In vitro cell-based experiments confirmed that the downregulation of TUG1 inhibits lens epithelial cell apoptosis. Mechanistically, Smac expression is negatively regulated by miR-29b. TUG1 competitively inhibits miR-29b expression and causes the release of more Smac. In addition, miR-29b reverses the effect of TUG1 on HLE-B3 cells. In conclusion, lncRNATUG1 increases Smac expression by competitively inhibiting miR-29b and promoting the apoptosis of lens epithelial cells in age-related cataracts. This mechanism is the cytological basis of ARC formation. Based on these results, the TUG1-miR29b-Smac axis may be a new molecular pathway to regulate the development of age-related cataracts.</p>
Genes with transcripts predicted to be miR-195 or miR-26b targets by all 5 predictive algorithms included in starBase, or experimentally identified as targets by pulldown assay
<p>Genes with transcripts predicted to be miR-195 or miR-26b targets by all 5 predictive algorithms included in starBase, or experimentally identified as targets by pulldown assay</p>
Data for FUV to MIR R(V) relationship paper
<p>Extinction curves used for the analysis presented in the paper titled "One Relation for All Wavelengths: The Far-Ultraviolet to Mid-Infrared Milky Way Spectroscopic R(V) Dependent Dust Extinction Relationship" by Gordon et al. (2023, ApJ, in press).</p>
Images for pdb entry 8BXR Titin FnIII-domain I109-I111 (I/A4-A/A6) from the MIR region
<p>Structure for 8BXR Titin FnIII-domain I109-I111 (I/A4-A/A6) from the MIR region calculated from these two merged data sets. </p>
Datasets for "GABAergic miR-34a regulates Dorsal Raphè inhibitory transmission in response to aversive, but not rewarding, stimuli"
<p>Datasets for "GABAergic miR-34a regulates Dorsal Raphè inhibitory transmission in response to aversive, but not rewarding, stimuli"</p>
Dataset of scientific article: "Effect of miR-34a on expression of clock and clock-controlled genes in human cancer DLD1 and Lovo cells with different backgrounds in respect to p53 functionality and 17β-estradiol-mediated regulation"
<p>The dataset includes "raw" data used for the calculation of gene expression, wound healing test, fluorescence intensity, and MTS test.</p> <p> </p>
Endogenous hsa-circ_0007113 binds hsa-miR-515-5p to regulate senescence in human embryonic lung fibroblasts
Open the record for dataset details and reuse information.
miR-142-3p as Potential Biomarker of Synaptopathy in MS
ClinicalTrials.gov study NCT03999788. IPD Sharing: Not stated. Countries: 1. Publications: 16.
A Dose Escalation Study of LNA-i-Mir-221 for Cancer Treatment
ClinicalTrials.gov study NCT04811898. IPD Sharing: NO. Countries: 1. Publications: 12.
A Multicenter Phase I Study of MRX34, MicroRNA miR-RX34 Liposomal Injection
ClinicalTrials.gov study NCT01829971. IPD Sharing: NO. Countries: 2. Publications: 2.
miR-155 Expression in Episodic and Chronic Migraine
ClinicalTrials.gov study NCT05891808. IPD Sharing: Not stated. Countries: 1. Publications: 10.
ScienceDex guides
Understand access before you commit
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.