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.
6,171
datasets available to search
ShareScore release 0.9.0
Dataset results
6,171 results for “mutant”
Diffraction images of crystals of the first and second spectrin repeats (mutant C420A/C435A) of human plectin (PDB code 2ODV): 2-wavelength SeMet MAD dataset
<p>Diffraction images of SeMet labeled crystals of a fragment of human plectin that includes the first and second spectrin repeats (SR1-SR2) of the plakin domain. The two Cys in the wild type sequence were replaced by Ala.</p> <p>This Se-Met MAD dataset was used for the <em>de novo</em> phasing of the pdb entry 2ODV (http://www.rcsb.org/pdb/explore/explore.do?structureId=2ODV).</p> <p> </p> <p>Data was collected at the BM14 beamline of the European Synchrotron Radiation Facility (ESRF, Grenoble, France) using a Mar CCD detector. Data from the same crystal were collected at two wavelengths :</p> <ul> <li>Remote wavelength (0.9185 Å): 180 images (1 degree oscillation per image).</li> <li>Peak wavelength ( 0.9785 Å): 360 images (1 degree oscillation per image).</li> </ul>
Raw band intensity values for ATG3 WT or Mutants in vitro LC3 lipidation
<p>Raw band intensity values used for the quantification of in vitro LC3 lipidation results (Fig4C) in Three-step docking by WIPI2, ATG16L1 and ATG3 delivers LC3 to the phagophore.</p>
Prediction and analysis of phenotypes in the Arabidopsis clock mutant prr7prr9 using the Framework Model v2 (FMv2)
<p>This upload contains or links to the biological data, FMv2 model and simulations for the Chew et al. 2017 paper (bioRxiv <a href="https://doi.org/10.1101/105437">https://doi.org/10.1101/105437</a> ), updated 2022 as bioRxiv <a href="https://doi.org/10.1101/105437v2">https://doi.org/10.1101/105437v2</a>, mostly testing and simulating the effect of a slow circadian clock in the <em>prr7prr9 </em>double mutant compared to the Col wild type plants, with controls in <em>lsf1 </em>and <em>prr7 </em>single mutants. This is one of the outputs from the EU TiMet project, <a href="https://fairdomhub.org/projects/92">https://fairdomhub.org/projects/92</a>.</p> <p>Several data files contain results generated in the same studies, but not covered by the publication. For example, additional time points (18 or 21 days of growth), many additional metabolites, and additional genotypes including <em>pgm</em>, <em>lhy cca1, </em>and in one case, <em>toc1 </em>and <em>gi</em>.</p> <p>This data archive was updated during submisson to the journal _in Silico _Plants in 2022, and is formatted as a Research Object, generated by the Snapshot function of FairdomHub, based on <a href="https://fairdomhub.org/investigations/123">Investigation https://fairdomhub.org/investigations/123.</a> The same Snapshot is shared on FairdomHub and will be from the University of Edinburgh Datashare.</p> <p>We request that users gives appropriate credit to the authors of any data released here, as a norm of academic practice, including data released under CC-0 licence on the FairdomHub.</p>
Spatial characterization of the motor and non-motor somal and axonal transcriptome in adult healthy and mutant FUS mice
<table> <tbody> <tr> <td> <p>Here we investigated the transcriptome of motor and non-motor axons and cell bodies in the context of mutant FUS-related amyotrophic lateral sclerosis (ALS). We applied Nanostring GeoMX Digital Spatial Profiler platform to profile the transcriptome of subcellular compartments in the lower motor circuitry of a mouse model ricapitulating ALS motor symptoms. This work sheds light for the first time on the transcriptomic alterations in axons and in somas which may contribute to axonal degeneration and neuromuscular junction denervation, early features of ALS.</p> </td> </tr> </tbody> </table>
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>
DATA ANALYSIS - SARS-COV-2 ( Del69-70 VARIANT ) – NEW UK MUTANTS
<p>The data for S - genome sequence analysis known as Del69-70 is under variant of concern ( VOC ) . It is also termed as variant of investigation ( VUI ) . The data for VUI is statistically analysed by datewise and regionwise . The software used for data analysis is CURVE FINDER V.1.4 . The reproducibility of correlation and standard error is reported here for analysis of scattered data an attempt to study the Rational Fit and Harris Fit .</p>
Diffraction images of crystals of the first and second spectrin repeats (mutant C420A/C435A) of human plectin (PDB code 2ODV)
<p>Diffraction images of a native crystals of a fragment of human plectin that includes the first and second spectrin repeats (SR1-SR2) of the plakin domain. The two Cys in the wild type sequence were replaced by Ala.</p> <p>Images correspond to the dataset used to refine the pdb entry 2ODV (http://www.rcsb.org/pdb/explore/explore.do?structureId=2ODV).</p> <p> </p> <p>Data was collected at the BM14 beamline of the European Synchrotron Radiation Facility (ESRF, Grenoble, France) using radiation of 0.9785 Å wavelength and a Mar CCD detector. The dataset consists of 360 images (1 degree oscillation per image). Data extend to ~1.85 Å resolution.</p>
Characterization of cefiderocol resistant spontaneous mutant variants of Klebsiella pneumoniae producing NDM-5 with single mutation in cirA
<p>Cefiderocol (CFDC) is a siderophore-cephalosporin antibiotic designed to combat highly resistant Gram-negative bacterial infections. Its mechanism involves a strong affinity for iron and active transport into bacterial cells, providing an alternative against strains resistant to common antibiotics. However, the emergence of CFDC resistance in Klebsiella is a growing concern. Recent reports highlight increasing CFDC resistance in K. pneumoniae, particularly associated with mutations in the cirA gene, responsible for encoding a siderophore receptor. Co-localization of blaNDM-like gene and cirA mutations correlates with higher CFDC resistance. The study focuses on a carbapenem-resistant K. pneumoniae strain (Kp-1) with carbapenemases blaNDM-5 and blaOXA-181, recovered from a post-surgery patient. The strain exhibited resistance to all tested antibiotics but susceptibility to CFDC. Heteroresistant populations with the halo on inhibition of CFDC were observed. Genomic analysis identified a novel mutation (W123*) in the cirA gene associated with CFDC resistance. Additionally, increased blaNDM-5 expression in Kp-1 IHC (intra-halo colony) compared to Kp-1 was noted. The coexistence of blaNDM-like and cirA variants, along with high blaNDM-5 expression, explains the observed 21-fold increase in Minimum Inhibition Concentration (MIC) in Kp-1 IHC. The study contributes to understanding the molecular mechanisms driving the emergence of cefiderocol resistance, emphasizing the significance of coexisting mutations in cirA and blaNDM-like genes.</p>
Spatially resolved metabolic composition in seeds of common bean: comparison of the low phytic acid mutant and the wild type
<p>Common bean (Phaseolus vulgaris L.) seeds are a good source of energy, are rich in proteins and carbohydrates, minerals and vitamins (such as Fe, Zn, B-vitamin), and bioactive compounds, such as polyphenols. However, the presence of some antinutritional compounds, such as phytic acid (PA), which decreases mineral bioavailability, can limit the nutritional value of common beans. Therefore, genotypes with low PA concentrations in common beans have been generated. The increased bioavailability of Fe from LPA mutant seeds compared to the wild type common beans was shown in a stable Fe-isotope absorption study in Swiss women, indicating that the seeds of LPA common bean could be used to help remedy the Fe malnutrition in women. Within this TNA project, we spatially resolved molecular composition in LPA mutant and wild-type common beans, particularly the distribution of PA. In total, three replicates of each genotype were analyzed with MeV-SIMS at RBI. Positive and negative modes were operated for analysis of the samples and of the standard (PA). Best spectra were obtained in negative mode, in which three distinct peaks were observed in the standard (PA): 63 m/z: PO2-, 79 m/z: PO3- and 97 m/z: H2PO4-.</p>
Multi-omic analysis of the Arabidopsis clock activator mutant rve 4 6 8 reveals connections to carbohydrate metabolism and proteasome regulation
<p>Plants are able to sense changes in their light environments, such as the onset of day and night, as well as anticipate these changes in order to adapt and survive. Central to this ability is the plant circadian clock, a molecular circuit that precisely orchestrates plant cell processes over the course of a day. REVEILLE proteins (RVEs) are recently discovered members of the plant circadian circuitry that activate the evening complex and PRR genes to maintain regular circadian oscillation. The RVE 8 protein and its two homologs, RVE 4 and 6, have been shown to limit the length of the circadian period, with rve 4 6 8 triple-knockout plants possessing an elongated period along with increased leaf surface area, biomass, cell size and delayed flowering relative to wild-type Col-0 plants. Here, using a multi-omics approach consisting of phenomics, transcriptomics, proteomics, and metabolomics we draw novel connections between RVE8-like proteins and a number of core plant cell processes. In particular, we reveal that loss of RVE8-like proteins results in altered carbohydrate, organic acid and lipid metabolism, including a starch excess phenotype at dawn. We further demonstrate that rve 4 6 8 plants have lower levels of 20S proteasome subunits and possess significantly reduced proteasome activity, potentially explaining the increase in cell-size observed in RVE8-like mutants. Overall, this robust, multi-omic dataset, provides substantial new insights into the far reaching impact RVE8-like proteins have on the diel plant cell environment.<br> <br> This dataset has the raw search outputs for the mass-spec analysis for this manuscript. </p>
X-Ray Diffraction data from Membrane transport protein AcrB, V612F mutant with bound minocycline, source of 9FHC structure
<p>Crystals were grown of the membrane transport protein AcrB, V612F mutant, with bound minocycline. </p> <p>X-ray diffraction data of this upload: 400 frames of 0.5° width were collected on 2007-04-30 at the X06SA beamline of Swiss Light Source at Paul-Scherrer-Institute (Switzerland).</p> <p>The data can be processed with XDS; XDS.INP is provided as part of the upload.</p> <p>The data are the basis of the PDB 9FHC structure.</p>
Assessment of mutation probabilities of KRAS G12 missense mutants and their long-time scale dynamics by atomistic molecular simulations and Markov state modeling: Datasets.
<p>Datasets related to the publication [1].<br> Including:</p> <ul> <li>KRAS G12X mutations derived from COSMIC v.79 [http://cancer.sanger.ac.uk/cosmic/] (KRAS_G12X_mut_COSMICv79..xlsx)</li> <li>RMSFs (300-2000ns) of GDP-systems (300_2000rmsf_GDP_systems_RAW_AVG_SE.xlsx)</li> <li>RMSFs (300-2000ns) of GTP-systems (300_2000RMSF_GTP_systems_RAW_AVG_SE.xlsx)</li> <li>PyInteraph analysis data for salt-bridges and hydrophobic clusters (.dat files for each system in the PyInteraph_data.zip-file)</li> <li>Backbone trajectories for each system (residues 4-164; frames for every 1ns). Last number (e.g. _1) refers to the replica of the simulated system.</li> <li>backbone_4-164.gro/.pdb/.tpr -files (resid 4-164) </li> </ul> <p><br> [1] Pantsar T et al. Assessment of mutation probabilities of KRAS G12 missense mutants and their long-time scale dynamics by atomistic molecular simulations and Markov state modeling. <em>PLoS Comput Biol Submitted</em> (2018)</p>
Molecular dynamics simulations of the interaction of the quadruple mutant human CYP2J2 (R111A + R117A + R382A + R446A) with arachidonic acid (POSES 1-3)
<p><strong>Description of files in this dataset:</strong></p> <p><strong>MD_quadmut_CYP2J2_AA_StateX_repeatY.zip</strong> : Series of zipped directories for molecular dynamics simulations of arachidonic acid in the active site of the quadruple R111A + R117A+R382A+R446A) mutant CYP2J2. X is the docking pose number that constitutes the starting point of the simulation (the 6 lowest-energy poses from docking were selected as the starting points of the simulations - this dataset is State(pose) 1). Y is the repeat (each simulation was repeated 3 times, hence there are 3 repeats per pose). </p> <p>Each directory contains the following sub-directories:</p> <p>001.leap : Amber parameter and coordinate files; PDBs; ligands; leap commands</p> <p>002.min : Minimisation stage</p> <p>003.heat : Heating stage</p> <p>004.equil: Equilibration stage</p>
Molecular dynamics simulations of the interaction of mutant human CYP2J2 (R117A) with arachidonic acid (POSES 5-6)
<p><strong>Description of files in this dataset:</strong></p> <p><strong>MD_mutR117A_CYP2J2_AA_StateX_repeatY.zip</strong> : Series of zipped directories for molecular dynamics simulations of arachidonic acid in the active site of the R117A mutant CYP2J2. X is the docking pose number that constitutes the starting point of the simulation (the 6 lowest-energy poses from docking were selected as the starting points of the simulations - this dataset is State(pose) 1). Y is the repeat (each simulation was repeated 3 times, hence there are 3 repeats per pose). </p> <p>Each directory contains the following sub-directories:</p> <p>001.leap : Amber parameter and coordinate files; PDBs; ligands; leap commands</p> <p>002.min : Minimisation stage</p> <p>003.heat : Heating stage</p> <p>004.equil: Equilibration stage</p> <p>005.md : Production stage</p> <p>006.analysis : Basic energy graphs</p> <p>007.cpptraj: Contains only the file strip.md.nc (Amber trajectories stripped of water in netCDF format)</p>
Homology modelling, molecular docking and molecular dynamics simulations of wild type and mutant human CYP2J2 with three polyunsaturated fatty acids
<p>This is the "parent" repository for the Data Note : "­Molecular dynamics simulations of the interaction of wild type and mutant human CYP2J2 with polyunsaturated fatty acids" by Abelak, Bishop-Bailey and Nobeli.</p> <p>It contains a document (<strong>Abelak_etal_Methods.pdf</strong>) describing the methods used to produce the data here and the data in all repositories supplementing it.</p> <p>It also contains a shell script (<strong>create_sim4_repeats.sh</strong>) that is typical of those used to set up the molecular dynamics simulations in the repositories supplementing this one.</p> <p>Finally, it contains the results of the homology modelling and docking simulations that formed the starting points for the molecular dynamics simulations in this study.</p> <p>Description of files in this dataset:</p> <p><strong>C2J2_min3_mod_noH.pdb</strong> : Homology model of the wild type CYP2J2 built from an alignment of templates with PDB ids: 1SUO, 2P85, 3EBS and 1Z10.</p> <p><strong>docking_wild_type_C2J2.zip</strong> : Nine docked poses of arachidonic acid docked to the homology model of the wild type CYP2J2.</p> <p>Details of how this data was produced is available in the Abelak_etal_Methods.docx document.</p>
Molecular dynamics simulations of the interaction of the double mutant human CYP2J2 (R117A and R111A) with arachidonic acid (POSES 1-3)
<p><strong>Description of files in this dataset:</strong></p> <p><strong>MD_mutR111A_R117A_CYP2J2_AA_StateX_repeatY.zip</strong> : Series of zipped directories for molecular dynamics simulations of arachidonic acid in the active site of the double R111A + R117A mutant CYP2J2. X is the docking pose number that constitutes the starting point of the simulation (the 6 lowest-energy poses from docking were selected as the starting points of the simulations - this dataset is State(pose) 1). Y is the repeat (each simulation was repeated 3 times, hence there are 3 repeats per pose). </p> <p>Each directory contains the following sub-directories:</p> <p>001.leap : Amber parameter and coordinate files; PDBs; ligands; leap commands</p> <p>002.min : Minimisation stage</p> <p>003.heat : Heating stage</p> <p>004.equil: Equilibration stage</p>
Molecular dynamics simulations of the interaction of mutant human CYP2J2 (R117A) with arachidonic acid (POSES 1-4)
<p><strong>Description of files in this dataset:</strong></p> <p><strong>MD_mutR117A_CYP2J2_AA_StateX_repeatY.zip</strong> : Series of zipped directories for molecular dynamics simulations of arachidonic acid in the active site of the R117A mutant CYP2J2. X is the docking pose number that constitutes the starting point of the simulation (the 6 lowest-energy poses from docking were selected as the starting points of the simulations - this dataset is State(pose) 1). Y is the repeat (each simulation was repeated 3 times, hence there are 3 repeats per pose). </p> <p>Each directory contains the following sub-directories:</p> <p>001.leap : Amber parameter and coordinate files; PDBs; ligands; leap commands</p> <p>002.min : Minimisation stage</p> <p>003.heat : Heating stage</p> <p>004.equil: Equilibration stage</p> <p>005.md : Production stage</p> <p>006.analysis : Basic energy graphs</p> <p>007.cpptraj: Contains only the file strip.md.nc (Amber trajectories stripped of water in netCDF format)</p>
Molecular dynamics simulations of the interaction of mutant human CYP2J2 (R111A) with arachidonic acid (POSES 4-6)
<p><strong>Description of files in this dataset:</strong></p> <p><strong>MD_mutR111A_CYP2J2_AA_StateX_repeatY.zip</strong> : Series of zipped directories for molecular dynamics simulations of arachidonic acid in the active site of the R111A mutant CYP2J2. X is the docking pose number that constitutes the starting point of the simulation (the 6 lowest-energy poses from docking were selected as the starting points of the simulations - this dataset is State(pose) 1). Y is the repeat (each simulation was repeated 3 times, hence there are 3 repeats per pose). </p> <p>Each directory contains the following sub-directories:</p> <p>001.leap : Amber parameter and coordinate files; PDBs; ligands; leap commands</p> <p>002.min : Minimisation stage</p> <p>003.heat : Heating stage</p> <p>004.equil: Equilibration stage</p> <p>005.md : Production stage</p> <p>006.analysis : Basic energy graphs</p> <p>007.cpptraj: Contains only the file strip.md.nc (Amber trajectories stripped of water in netCDF format)</p>
Molecular dynamics simulations of the interaction of the quadruple mutant human CYP2J2 (R111A + R117A + R382A + R446A) with arachidonic acid (POSES 4-6)
<p><strong>Description of files in this dataset:</strong></p> <p><strong>MD_quadmut_CYP2J2_AA_StateX_repeatY.zip</strong> : Series of zipped directories for molecular dynamics simulations of arachidonic acid in the active site of the quadruple (R111A + R117A+R382A+R446A) mutant CYP2J2. X is the docking pose number that constitutes the starting point of the simulation (the 6 lowest-energy poses from docking were selected as the starting points of the simulations - this dataset is State(pose) 1). Y is the repeat (each simulation was repeated 3 times, hence there are 3 repeats per pose). </p> <p>Each directory contains the following sub-directories:</p> <p>001.leap : Amber parameter and coordinate files; PDBs; ligands; leap commands</p> <p>002.min : Minimisation stage</p> <p>003.heat : Heating stage</p> <p>004.equil: Equilibration stage</p>
The LAVA mutants defective in auxin-regulated primary or lateral root development.
<p><span>Regulation of PIN activity, polarity as well as auxin gradient generation and its canalisation remain crucial topics in plant developmental biology especially in the context of organogenesis like the formation new lateral roots. Here, we are presenting the LAVA (LR Alterations Visualised after Auxin) collection of 278 mutants, defective in auxin-induced lateral root (LR) morphogenesis. Those mutants were obtained from a forward genetic screen in which synthetic auxin 1-Naphtyl Acetic Acid (1-NAA) was used to induce LR formation in the mutagenized PIN3::PIN3-GFP population. Our database contains mutant root phenotyping and for a subset of the collection, we recorded PIN polarity and subcellular trafficking, cotyledon vasculature development, primary and LR gravitropism as well as aerial phenotypes with some reminiscent to auxin-regulated organogenesis aberrations. We are convinced that our dataset can serve as a unique tool to identify novel components of auxin signalling, transport, and cell polarity but also be of interest to the broader plant research community interested in the roots system architecture that is vital for plant survival, growth and adaptation to environmental conditions.</span></p> <p><span>The phenotype analysis of the mutant collection is summarized and organised in an Excel spreadsheet (2024-08-07_mutant_database_Table S1). The photographic material is organised in folder form (see Supporting Data S1 in this repository), where each folder number corresponds to a particular mutant and entry in the excel table.</span></p> <p><span> Mutant seeds will be available in the European Arabidopsis Stock Centre (NASC). The seed sending to the repository is in progress. </span></p> <p><span>The manuscript describing this work is currently being submitted to the research journal. Its version will be available on the open access Masaryk University repository.</span></p>
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.