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.
35
datasets available to search
ShareScore release 0.9.0
Dataset results
35 results for “GRN”
Synthetic datasets reflecting the shRNA-seq knockdown ENCODE data for HepG2 and K562 with coresponding GRN
<p>Synthetic data correspond to the ENCODE data for cell lines HepG2 (https://www.encodeproject.org/biosamples/ENCBS282XVK/) and K562 (https://www.encodeproject.org/biosamples/ENCBS023XVB/). The data and networks were generated using GeneSPIDER (publicly available at https://bitbucket.org/sonnhammergrni/genespider/).</p> <p> </p> <p><strong>Table.1 </strong>Description of the files</p> <table> <tbody> <tr> <td>data_HepG2like_SNR_L=0.0054699_diff=1.6188e-05.txt</td> <td>Synthetic gene expression knockdown (shRNA-seq) data immitating the ENCODE data for HepG2 cell line. Data size: 232 RBPs vs 464 experiments (2 replicates). SNR_L is the value of signal to noise ratio. Difference (diff) value tells the difference between replicate correlation coefficients of real and synthetic ENCODE data. Columns represent experiments, rows represent genes.</td> </tr> <tr> <td>data_K562like_SNR_L=0.0028692_diff=0.00017339.txt</td> <td>Synthetic gene expression knockdown (shRNA-seq) data immitating the ENCODE data for K562 cell line. Data size: 232 RBPs vs 464 experiments (2 replicates). SNR_L is the value of signal to noise ratio. Difference (diff) value tells the difference between replicate correlation coefficients of real and synthetic ENCODE data. Columns represent experiments, rows represent genes.</td> </tr> <tr> <td>network_HEPG2like_sparsity4.txt</td> <td>Synthetic scale-free gene regulatory network compatibile with data_HepG2like_SNR_L=0.0054699_diff=1.6188e-05.txt. Sparsity (average node degree) is 4 including selfloops. Direction should be read from columns to rows.</td> </tr> <tr> <td>network_K562like_sparsity4.txt</td> <td>Synthetic scale-free gene regulatory network compatibile with data_K562like_SNR_L=0.0028692_diff=0.00017339.txt. Sparsity (average node degree) is 4 including selfloops. Direction should be read from columns to rows.</td> </tr> <tr> <td>perturbations_HepG2&K562_2replicates.txt</td> <td>Perturbation matrix including information about knockeddown RBPs. Data size: 232 RBPs vs 464 experiments (2 replicates).</td> </tr> </tbody> </table> <p> </p> <p>Created by Garbulowski et al. (2024) as a part of the work entitled "Comprehensive analysis of the RBP regulome reveals functional modules and drug candidates in liver cancer"</p>
GRN-AV-traffic-entity
<p>The GRN-AV-traffic-entity dataset is a collection of labelled multi-modal synched audio-video (AV) data, which is labelled with traffic sounds (e.g., engine noise, wheel rolling and vehicle horn). The video frames are not labelled, but are included.</p>
GRN-AV-traffic-state
<p>This GRN-AV-traffic-state dataset is a collection of labelled multi-modal data for the purpose of training audio classification models </p>
GRN_MARVEL_MULTIMODAL_DATASET
<p>The raw audio-video data was collected from Mgarr, a rural town on the western coast from IP cameras. Data has been manually annotated for bicycles, pedestrians and motorcycles. Annotation is in the form of labelling sound events and bounding boxes for entities of interest.</p>
GRN_MARVEL_ANOMALOUS_TRAJECTORIES
<p>The raw audio-video data was collected from Mgarr, a rural town on the western coast from IP cameras. Data has been manually annotated for anomalous trajectories. Annotation data in the form of a CSV file.</p>
GRN_MARVEL_AUDIO_VISUAL_CROWD_COUNTING
<p>The raw audio-video data was collected from Mgarr, a rural town on the western coast from IP cameras. Data has been manually annotated for pedestrians.</p>
GRN-TXT-traffic-data
<p>This dataset is generated from the GDPR compliant AI models developed in MARVEL (objective 2) and/or GRN’s proprietary CATFlow system. These models take as input the audio or video streams and output non-binary structured data, which is further processed in the implementation of some use-cases.</p>
Knockout of liver fluke granulin, Ov-grn-1, impedes malignant transformation during chronic infection with Opisthorchis viverrini: BrdU staining and fibrosis
<p>Knockout of liver fluke granulin, Ov-grn-1, impedes malignant transformation during chronic infection with Opisthorchis viverrini:</p> <p>1. BrdU stained images for the detection of proliferation with manual counting of brown stained cell proportion. Each group in a seperate file BRDUxxx</p> <p>2. Fibrosis local images stained with Sirius red with automated analysis with imageJ. Grouped into one zip file</p> <p>3. Global analysis of liver fibrosis pathogenesis (Ishak scores) performed by 2 blinded pathologists. Grouped into one zip file</p> <p>Methods in associated publication. Briefly 3 groups of 15 hamsters were infected with 100 NEJ flukes that had been gene edited with CRISPR/Cas9 plasmids targeting either Ov-grn-1, Ov-tsp-2, or a scrambled sequence as the control group. Images in these files are the micrographs from these three groups of hamsters. Numbered 1-15 representing the hamster and left/middle/right representing the liver lobe the section was taken from.</p> <p> </p> <p>Knockout of liver fluke granulin, Ov-grn-1, impedes malignant transformation during chronic infection with Opisthorchis viverrini</p> <p>ABSTRACT: Infection with the food-borne liver fluke <em>Opisthorchis viverrini</em> is the principal risk factor for cholangiocarcinoma (CCA) in the Mekong Basin countries of Thailand, Lao PDR, Vietnam, Myanmar and Cambodia. Using a novel model of CCA, involving infection with gene-edited liver flukes in the hamster during concurrent exposure to dietary nitrosamine, we explored the role of the fluke granulin-like growth factor <em>Ov</em>-GRN-1 in malignancy. We derived RNA-guided gene knockout flukes (<em>ΔOv-grn-1)</em> using CRISPR/Cas9/gRNA materials delivered by electroporation. Genome sequencing confirmed programmed Cas9-catalyzed mutations of the targeted genes, which was accompanied by rapid depletion of transcripts and the proteins they encode. Gene-edited parasites colonized the biliary tract of hamsters and developed into adult flukes. However, less hepatobiliary tract disease manifested during chronic infection with <em>ΔOv-grn-1</em> worms in comparison to hamsters infected with control gene-edited and mock-edited parasites. Specifically, immuno- and colorimetric-histochemical analysis of livers revealed markedly less periductal fibrosis surrounding the flukes and less fibrosis globally within the hepatobiliary tract during infection with <em>ΔOv-grn-1</em> genotype worms, minimal biliary epithelial cell proliferation, and significantly fewer mutations of <em>TP53</em> in biliary epithelial cells. Moreover, fewer hamsters developed high-grade CCA compared to controls. The clinically relevant, pathophysiological phenotype of the hepatobiliary tract confirmed a role for this secreted growth factor in malignancy and morbidity during opisthorchiasis.</p>
Deficiency of GRN, a frontotemporal dementia gene, results in gangliosidosis
<p>Haploinsufficiency of <em>GRN</em> causes frontotemporal dementia (FTD). The <em>GRN</em> locus produces progranulin (PGRN), which is cleaved to lysosomal granulin polypeptides. The function of lysosomal granulins and why their absence causes neurodegeneration are unclear. Here we discover that PGRN-deficient human cells and murine brains, as well as human frontal lobes from <em>GRN</em>-mutation FTD patients have increased levels of gangliosides, glycosphingolipids that contain sialic acid. In these cells and tissues, levels of lysosomal enzymes that catabolize gangliosides were normal, but levels of bis(monoacylglycero)phosphates (BMP), lipids required for ganglioside catabolism, were reduced with PGRN deficiency. Our findings indicate that granulins are required to maintain BMP levels to support ganglioside catabolism, and that PGRN deficiency in lysosomes leads to gangliosidosis. Lysosomal ganglioside accumulation may contribute to neuroinflammation and neurodegeneration susceptibility observed in FTD due to PGRN deficiency and other neurodegenerative diseases.</p>
Data from: Primary progressive aphasias and GRN mutations
<p><strong>Objective:</strong> To determine relative frequencies and linguistic profiles of primary progressive aphasia (PPA) variants associated with progranulin (GRN) mutations, and study their neuroanatomical correlates.</p> <p><strong>Methods:</strong> PPA patients carrying GRN mutations (PPA-GRN) were selected amongst a national prospective research cohort of 1,696 frontotemporal dementia (FTD) patients, including 235 patients with PPA. All PPA patients with amyloid-positive CSF biomarkers were excluded. In this cross-sectional study, speech/language and cognitive profiles were characterized with standardized evaluations, and grey matter (GM) atrophy patterns using voxel-based morphometry. Comparisons were performed with controls, and sporadic PPA patients.</p> <p><strong>Results:</strong> Among the overall population of 235 patients, 45 (19%) carried GRN mutations. We studied 32 of these and showed that logopenic PPA (lvPPA) was the most frequent linguistic variant (13, 41%), followed by non-fluent/agrammatic (nfvPPA: 9, 28%) and mixed forms (8, 25%). Semantic variant was rather rare (2, 6%). LvPPA patients, qualified as non-amyloid-lvPPA, presented canonical logopenic deficit. Seven out of 13 had a pure form, six showed subtle additional linguistic deficits not fitting criteria for mixed PPA, hence labelled as "logopenic-spectrum variant". GM atrophy primarily involved left posterior temporal gyrus, mirroring neuroanatomical changes of amyloid-positive-lvPPA. NfvPPA patients presented agrammatism (89%) rather than apraxia of speech (11%).</p> <p><strong>Conclusions:</strong> This study shows that most frequent PPA variant associated with GRN mutations is non-amyloid lvPPA, preceding nfvPPA and mixed forms, and illustrates that language network may be affected at different levels. GRN testing is indicated for PPA patients, whether familial or sporadic. This finding is important for upcoming GRN gene-specific therapies.</p>
Dataset for paper "GRN-Transformer: Predicting Single Cell Gene Regulatory Network based on Axial Transformer"
<p>Dataset for paper "GRN-Transformer: Predicting Single Cell Gene Regulatory Network based on Axial Transformer"</p>
ASO-mediated knockdown of GPNMB in mutant-GRN and Grn-deficient peripheral myeloid cells disrupts lysosomal function and immune responses
<p><strong>Background: </strong>Increases in GPNMB are detectable in FTD-<em>GRN</em> cerebrospinal fluid (CSF) and post-mortem brain, and brains of aged <em>Grn</em>-deficient mice. Although no upregulation of GPNMB is observed in the brains of young <em>Grn</em>-deficient mice, peripheral immune cells of these mice do exhibit this increase in GPNMB. Importantly, the functional significance of GPNMB upregulation in progranulin-deficient states is currently unknown. Given that GPNMB has been discussed as a potential therapeutic target in <em>GRN</em>-mediated neurodegeneration, it is vital for the field to determine what the normal function of GPNMB is in the immune system, and whether targeting GPNMB will elicit beneficial or deleterious effects.</p> <p><strong>Methods: </strong>The effects of GPNMB knock-down via antisense oligonucleotide (ASO) were assessed in peripheral blood mononuclear cells (PBMCs) from 25 neurologically healthy controls (NHCs) and age- and sex-matched FTD-<em>GRN </em>patients, as well as peritoneal macrophages (pMacs) from progranulin-deficient (<em>Grn</em><sup>-/-</sup>) and B6 mice. Lysosomal function, antigen presentation and MHC-II processing and recycling were assessed, as well as cytokine release and transcription.</p> <p><strong>Results: </strong>We demonstrate here that ASO-mediated knockdown of GPNMB increases lysosomal burden and cytokine secretion in FTD-GRN carrier and neurologically healthy controls (NHCs) monocytes. <span>ASO-mediated knockdown of GPNMB in <em>Grn</em>-deficient macrophages decreased lysosomal pan-cathepsin activity and protein degradation. In addition, </span>ASO-mediated knockdown of GPNMB increased MHC-II surface expression, which was driven by decreased MHC-II uptake and recycling, in macrophages from <em>Grn</em>-deficient females. Finally, ASO-mediated knockdown of GPNMB dysregulated IFN<span><span><span>g</span></span>-stimulated cytokine transcription and secretion by mouse macrophages due to the absence of regulatory actions of the GPNMB extracellular fragment (ECF). </span></p> <p><strong>Conclusions: </strong><span>Our data herein reveals that </span>GPNMB has a regulatory effect on multiple immune effector functions, including capping inflammation and immune responses in myeloid cells via secretion of its ECF. Therefore, in progranulin-deficient states, the drastic upregulation in GPNMB transcript and protein may represent a compensatory mechanism to preserve lysosomal function in myeloid cells. These novel findings indicate that targeted depletion in FTD-<em>GRN</em> would not be a rational therapeutic strategy because it is likely to dysregulate important immune cell effector functions.</p>
Phase 1/2 Clinical Trial of LY3884963 in Patients With Frontotemporal Dementia With Progranulin Mutations (FTD-GRN)
ClinicalTrials.gov study NCT04408625. IPD Sharing: Not stated. Countries: 6. Publications: 2.
A First in Human Study in Healthy Volunteers and in Participants With Frontotemporal Dementia With Granulin (GRN) Mutation
ClinicalTrials.gov study NCT03636204. IPD Sharing: Not stated. Countries: 3. Publications: 1.
Data from: Primary progressive aphasias and GRN mutations
Open the record for dataset details and reuse information.
CDX2 dose-dependently influences the GRN underlying vascularization in human extraembryonic mesoderm-like cells
GEO Series GSE251813. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
Neurovascular dysfunction in GRN-associated frontotemporal dementia identified by single-nucleus RNA-sequencing of human cerebral cortex
GEO Series GSE163122. Homo sapiens. 93 samples. Type: Expression profiling by high throughput sequencing.
GRN knockout, sorted brain cells
GEO Series GSE78747. Mus musculus. 29 samples. Type: Expression profiling by high throughput sequencing.
GRN-1201 With Pembrolizumab in Subjects With Metastatic PD-L1+ NSCLC
ClinicalTrials.gov study NCT03417882. IPD Sharing: UNDECIDED. Countries: 1. Publications: 0.
Dose Finding Study of Nimodipine for the Treatment of Progranulin Insufficiency From GRN Gene Mutations
ClinicalTrials.gov study NCT01835665. IPD Sharing: UNDECIDED. Countries: 1. Publications: 0.
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.