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408 results for “ubiquitin”
Data set for "Analysis of the Ub to Ub-CR transition in ubiquitin"
<p>Data set for "Analysis of the Ub to Ub-CR transition in ubiquitin" containing the data bases for the wild type and the four mutants analysided, for use with PATHSAMPLE (http://www-wales.ch.cam.ac.uk/PATHSAMPLE.2.1.doc/PATHSAMPLE.html)</p>
Evolution of ubiquitin, cytoskeleton, and vesicular trafficking machinery in giant viruses
<p>This repository contains genomes, proteins, and alignments used in the study "Evolution of ubiquitin, cytoskeleton, and vesicular trafficking machinery in giant viruses".</p> <p> </p>
Ubiquitin Ligase Wwp1 Gene Deletion Attenuates Diastolic Dysfunction in Pressure Overload Hypertrophy
<p><strong><em>Background.</em></strong> Heart failure with a preserved left ventricular (LV) ejection fraction (HFpEF) often arises from a prolonged LV pressure overload (LVPO) and accompanied by abnormal extracellular matrix (ECM) accumulation. The E3 ubiquitin ligase WWP1 is a fundamental determinant ECM turnover. We tested the hypothesis that genetic ablation of<em> Wwp1</em> would alter the progression of LVPO induced HFpEF.</p> <p><strong><em>Methods/Results</em></strong><em>.</em> LV echocardiography in mice with global <em>Wwp1</em> deletion (n=41; <em>Wwp1<sup>-/-</sup></em>) was performed at 12 weeks of age (Baseline) and then at 2 and 4 weeks following LVPO (transverse aortic banding) or surgery without LVPO induction. Age-matched wild type mice (<em>Wwp1<sup>+/+</sup></em>; n=33) underwent identical protocols. LV EF remained constant and unchanged with LVPO and LV mass increased in both groups but was lower in the <em>Wwp1<sup>-/-</sup></em> mice. With LVPO, the E/A ratio, an index of LV filling, was 3.97 + 0.46 in <em>Wwp1<sup>+/+</sup></em> but was 1.73 + 0.19 in the <em>Wwp1<sup>-/-</sup></em> group (p<0.05). At the transcriptional level, mRNA for fibrillar collagens (types I and III) decreased by approximately 50% in <em>Wwp1<sup>-/-</sup></em> compared to the <em>Wwp1<sup>+/+</sup></em> group at 4 weeks post-LVPO (p<0.05) and was paralleled by a similar difference in LV fibrillar collagen content as measured by histochemistry. Moreover, mRNA levels for determinants favoring ECM accumulation, such as transforming growth factor (TGF) increased with LVPO, but were lower in the <em>Wwp1<sup>-/-</sup></em> group.</p> <p><strong><em>Summary.</em></strong> The absence of <em>Wwp1</em> reduced the development of LVH and subsequent progression to HFpEF. Modulating the WWP1 pathway could be a therapeutic target to alter the natural history of HFpEF.</p>
O-GlcNAc transferase OGT-1 and the ubiquitin ligase EEL-1 modulate seizure susceptibility in C. elegans Dataset
<p>Neurodevelopmental disorders such as epilepsy and autism have been linked to an imbalance of excitation and inhibition (E/I) in the central nervous system. The simplicity and tractability of<i> C. elegans</i> allows our electroconvulsive seizure (ES) assay to be used as a behavioral readout of the locomotor circuit and neuronal function. <i>C. elegans</i> possess conserved nervous system features such as gamma-aminobutyric acid (GABA) and GABA receptors in inhibitory neurotransmission, and acetylcholine (Ach) and acetylcholine receptors in excitatory neurotransmission. Our previously published data has shown that decreasing inhibition in the motor circuit, via GABAergic manipulation, will extend the time of locomotor recovery following electroshock. Similarly, mutations in a HECT E3 ubiquitin ligase called EEL-1 leads to impaired GABAergic transmission, E/I imbalance and altered sensitivity to electroshock. Mutations in the human ortholog of EEL-1, called HUWE1, are associated with both syndromic and non-syndromic intellectual disability. Both EEL-1 and its previously established binding protein, OGT-1, are expressed in GABAergic motor neurons, localize to GABAergic presynaptic terminals, and function in parallel to regulate GABA neuron function. In this study, we tested behavioral responses to electroshock in wildtype, <i>ogt-1</i>, <i>eel-1</i> and <i>ogt-1; eel-1</i> double mutants. Both <i>ogt-1 </i>and <i>eel-1 </i>null mutants have decreased inhibitory GABAergic neuron function and increased electroshock sensitivity. Consistent with EEL-1 and OGT-1 functioning in parallel pathways, <i>ogt-1; eel-1 </i>double mutants showed enhanced electroshock susceptibility. Expression of OGT-1 in the <i>C. elegans </i>nervous system rescued enhanced electroshock defects in <i>ogt-1; eel-1 </i>double mutants. Application of a GABA agonist, Baclofen, decreased electroshock susceptibility in all animals. Our <i>C. elegans</i> electroconvulsive seizure assay was the first to model a human X-linked Intellectual Disability (XLID) associated with epilepsy and suggests a potential novel role for the OGT-1/EEL-1 complex in seizure susceptibility.</p>
The midnolin-proteasome pathway catches proteins for ubiquitination-independent degradation
<p class="MsoNormal">Cells use ubiquitin to mark proteins for proteasomal degradation. While the proteasome also eliminates proteins that are not modified by ubiquitin, how this occurs mechanistically is unclear. We show here that midnolin promotes the destruction of many nuclear proteins including transcription factors encoded by the immediate-early-genes. Diverse environmental cues induce midnolin and its overexpression is sufficient to cause the degradation of its targets by a mechanism, which, remarkably, does not require ubiquitination. Instead, midnolin associates with the proteasome via <span>an alpha</span><span>-helix</span>, employs its Catch-domain to bind a region within substrates that adopts a beta-strand conformation, and uses a ubiquitin-like-domain to promote substrate destruction. Thus, midnolin contains three regions that function in concert to target a large set of nuclear proteins to the proteasome for degradation. </p>
Diagnostic Role of Serum Testican and Ubiquitin Levels in Patients With Head Trauma
ClinicalTrials.gov study NCT06537713. IPD Sharing: NO. Countries: 1. Publications: 14.
O-GlcNAc transferase OGT-1 and the ubiquitin ligase EEL-1 modulate seizure susceptibility in C. elegans Dataset
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The midnolin-proteasome pathway catches proteins for ubiquitination-independent degradation
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The Ubiquitin Ligase WWP1 Contributes to Shifts in Matrix Proteolytic Profiles and a Myocardial Aging Phenotype with Diastolic Heart Failure
<p><strong><em>Aims</em></strong>. Ubiquitylation is a key event that regulates protein turnover, and induction of the ubiquitin ligase E3 WWP1 has been associated with age. Left ventricular hypertrophy (LVH) commonly occurs as a function of age and can cause heart failure with a preserved ejection fraction (EF; HFpEF). We hypothesized that overexpression (O/E) of WWP1 in the heart would cause LVH as well as functional and structural changes consistent with the aging HFpEF phenotype.</p> <p><strong><em>Methods and Results.</em></strong> Global WWP1 O/E was achieved in mice (n=11) and echocardiography (40 MHz) performed to measure LV mass, EF, Doppler velocities (early-E, late/atrial-A), myocardial relaxation (E’), and isovolumetric relaxation time (IVRT) at 4, 6, and 8 weeks. Age matched wild type animals (n=15) were included as referent controls. LV EF was identical (60+1% vs 60+1%, p>0.90) with no difference in LV mass (67+3 vs 75+5, p>0.25) at 4 weeks. However, at 8 weeks of age, LV mass increased by over two-fold, E/A fell (impaired passive filling), and E/E’ was lower and IVRT prolonged (impaired LV relaxation) - all p<0.05. Collagen percent area increased by over two-fold and fibrillar collagen expression (rtPCR) by over 1.5 fold (p<0.05) with WWP1 O/E. WWP1 with an anti-WWP1 antibody could be identified in isolated cardiac fibroblasts with WWP1 increased by over two-fold in O/E fibroblasts (p<0.05).</p> <p><strong><em>Conclusion.</em></strong> Inducing WWP1 expression caused LVH, preserved systolic function, but impaired diastolic dysfunction, consistent with the HFpEF phenotype. Targeting the WWP1 pathway may be a novel therapeutic target for this intractable form of HF associated with aging.</p>
Data from: The UBR-1 ubiquitin ligase regulates glutamate metabolism to generate coordinated motor pattern in Caenorhabditis elegans
UBR1 is an E3 ubiquitin ligase best known for its ability to target protein degradation by the N-end rule. The physiological functions of UBR family proteins, however, remain not fully understood. We found that the functional loss of C. elegans UBR-1 leads to synchronized motor neuron activation, preventing body bending when animals generate reversal movements. This motor deficit is rescued by removing GOT-1, a transaminase that converts aspartate to glutamate. Both UBR-1 and GOT-1 are critically required in premotor interneurons of the reverse motor circuit to regulate the motor pattern. ubr-1 and got-1 mutants exhibit elevated and decreased glutamate level, respectively. These results raise an intriguing possibility that UBR proteins regulate glutamate metabolism.
15N-HSQC spectra of tagged Ubiquitin S57C
<p>15N-HSQC spectra of Ubiquitin S57C tagged with different lanthanide tags (C1, C2, C12 and C13)</p>
Source Data for: VCP/p97-Associated Proteins are Binders and Debranching Enzymes of K48-K63-Branched Ubiquitin Chains
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LC-MS analysis raw data of DTX3L-mediated enzymatic conjugation of ubiquitin with various nucleotide substrates
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USP5 Ubiquitin-Rhodamine110 Catalytic Activity Assay
<p>A ubiquitin-rhodamine110 assay was used to determine if ZnF-UBD ligands antagonize USP5 deubiquitinase (DUB) activity </p>
Supporting Data - Temperature and immunostimulants modulate transcription of the ubiquitin and apoptosis pathways in the Antarctic Harpagifer antarcticus and sub-Antarctic Harpagifer bispinis
<p>C<sub>t</sub> values obtained from Real-Time PCR (<em>ß-ACTIN</em>, <em>UBE3</em>, <em>SMAC/DIABLO</em> and <em>BAX</em> genes) of cDNA from liver, gills and spleen of <em>Harpagifer antarcticus</em> and <em>Harpagifer bispinis</em> fish stimulated with LPS, Poly I:C or non-stimulated (control, PBS-injected) under three temperatures (2, 5 and 8°C).</p>
Data from: The UBR-1 ubiquitin ligase regulates glutamate metabolism to generate coordinated motor pattern in Caenorhabditis elegans
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Data from: A genomic survey of HECT ubiquitin ligases in eukaryotes reveals independent expansions of the HECT system in several lineages.
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YTHDC1 affects the ubiquitination level of RAD51 by negatively regulating UBE3A expression and inhibits colorectal cancer cells apoptosis
GEO Series GSE245860. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
SIAH ubiquitin E3 ligases as modulators of inflammatory gene expression
GEO Series GSE179190. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing.
The E3 Ubiquitin Ligase Nedd4L Acts as a Checkpoint Against Activation in Quiescent Muscle Stem Cells
GEO Series GSE230622. Mus musculus. 19 samples. Type: Genome binding/occupancy profiling by high throughput sequencing; Expression profiling by high throughput sequencing.
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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.