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2,709 results for “mouse models”
Fly and mouse tracking models and kinematics related to Anipose toolkit paper
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Data from: Nanotransfection-based vasculogenic cell reprogramming drives functional recovery in a mouse model of ischemic stroke
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Cadmium exposure persistently modulates the gut-liver axis in an Alzheimer’s disease mouse model
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The KRASG12C Inhibitor MRTX849 Provides Insight toward Therapeutic Susceptibility of KRAS-Mutant Cancers in Mouse Models and Patients
<p>We directly interrogated the role of selected genes in mediating therapeutic response to MRTX849 utilizing a focused CRISPR/Cas9 knockout screen targeting approximately 400 genes including many genes involved in KRAS signaling. This was conducted in H358 and H2122 cells in vitro and in H2122 xenografts in vivo in presence and absence of MRTX849 treatment.</p> <p>Three independent drug anchored CRISPR studies were performed and two data files have been provided for each study. The .csv metadata files contain sample IDs, replicate number, sample descriptions and various experimental conditions. The .xlsx data files contain guide labels, guide sequences and NGS guide counts.Three independent drug anchored CRISPR studies were performed and two data files have been provided for each study. The .csv metadata files contain sample IDs, replicate number, sample descriptions and various experimental conditions. The .xlsx data files contain guide labels, guide sequences and NGS guide counts.</p>
3D models of mouse embryonic development (stl, converted from EMAP)
<p>A collection of readily-usable volumetric models for all tissues and stages of mouse peri-implantation development as extracted from the eMouse Atlas Project (E5.0 to E9.0), as well as custom-made models of all pre-implantation stages (E0 to E4.0). These models have been converted to a commonly used 3D format (.stl), and are provided in ready-made files for digital exploration and illustration.</p> <p>Specifically:</p> <ol> <li>individual .stl models of embryonic subcomponents for each developmental stage (e.g. epiblast, visceral endoderm; 1 folder per EMAP embryonic stage)</li> <li>ready-made .blend files where such components have been reassembled as a full embryo model, and in a scene with pre-prepared light sources and aligned camera (1 file per embryonic stage)</li> <li>a .blend file with all embryonic models provided arranged in a temporal lineup; and a .blend file with a "starter-pack" of pre-made materials to use for easy illustration.</li> </ol> <p>Also included are two data tables:</p> <ol> <li>"EMAP_key.xlsx" indicating the source of its model, and the embryonic stage corresponding to each Theiler Stage</li> <li> "EMAP_partslist.xlsx" containing the original name of each embryonic component provided (as used in <a href="https://www.emouseatlas.org/emap/ema/home.php">EMAP</a>), and the corresponding name used in this dataset.</li> </ol>
Mesenchymal stem cell-derived extracellular vesicles reduce senescence and extend healthspan in mouse models of aging.
<p>Source data file</p>
Data from: Correlations of behavioral deficits with brain pathology assessed through longitudinal MRI and histopathology in the HDHQ150/Q150 mouse model of Huntington's disease
A variety of mouse models have been developed that express mutant huntingtin (mHTT) leading to aggregates and inclusions that model the molecular pathology observed in Huntington's disease. Here we show that although homozygous HdhQ150 knock-in mice developed motor impairments (rotarod, locomotor activity, grip strength) by 36 weeks of age, cognitive dysfunction (swimming T maze, fear conditioning, odor discrimination, social interaction) was not evident by 94 weeks. Concomitant to behavioral assessments, T2-weighted MRI volume measurements indicated a slower striatal growth with a significant difference between wild type (WT) and HdhQ150 mice being present even at 15 weeks. Indeed, MRI indicated significant volumetric changes prior to the emergence of the "clinical horizon" of motor impairments at 36 weeks of age. A striatal decrease of 27% was observed over 94 weeks with cortex (12%) and hippocampus (21%) also indicating significant atrophy. A hypothesis-free analysis using tensor-based morphometry highlighted further regions undergoing atrophy by contrasting brain growth and regional neurodegeneration. Histology revealed the widespread presence of mHTT aggregates and cellular inclusions. However, there was little evidence of correlations between these outcome measures, potentially indicating that other factors are important in the causal cascade linking the molecular pathology to the emergence of behavioral impairments. In conclusion, the HdhQ150 mouse model replicates many aspects of the human condition, including an extended pre-manifest period prior to the emergence of motor impairments.
Data from: Characterization of leukemia-inducing genes using a proto-oncogene/homeobox gene retroviral human cDNA library in a mouse in vivo model
The purpose of this research is to develop a method to screen a large number of potential driver mutations of acute myeloid leukemia (AML) using a retroviral cDNA library and murine bone marrow transduction-transplantation system. As a proof-of-concept, murine bone marrow (BM) cells were transduced with a retroviral cDNA library encoding well-characterized oncogenes and homeobox genes, and the virus-transduced cells were transplanted into lethally irradiated mice. The proto-oncogenes responsible for leukemia initiation were identified by PCR amplification of cDNA inserts from genomic DNA isolated from leukemic cells. In an initial screen of ten leukemic mice, the MYC proto-oncogene was detected in all the leukemic mice. Of ten leukemic mice, 3 (30%) had MYC as the only transgene, and seven mice (70%) had additional proto-oncogene inserts. We repeated the same experiment after removing MYC-related genes from the library to characterize additional leukemia-inducing gene combinations. Our second screen using the MYC-deleted proto-oncogene library confirmed MEIS1and the HOX family as cooperating oncogenes in leukemia pathogenesis. The model system we introduced in this study will be valuable in functionally screening novel combinations of genes for leukemogenic potential in vivo, and the system will help in the discovery of new targets for leukemia therapy.
Data from: Overexpression of Dyrk1A is implicated in several cognitive, electrophysiological and neuromorphological alterations found in a mouse model of Down syndrome
Down syndrome (DS) phenotypes result from the overexpression of several dosage-sensitive genes. The DYRK1A (dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A) gene, which has been implicated in the behavioral and neuronal alterations that are characteristic of DS, plays a role in neuronal progenitor proliferation, neuronal differentiation and long-term potentiation (LTP) mechanisms that contribute to the cognitive deficits found in DS. The purpose of this study was to evaluate the effect of Dyrk1A overexpression on the behavioral and cognitive alterations in the Ts65Dn (TS) mouse model, which is the most commonly utilized mouse model of DS, as well as on several neuromorphological and electrophysiological properties proposed to underlie these deficits. In this study, we analyzed the phenotypic differences in the progeny obtained from crosses of TS females and heterozygous Dyrk1A (+/−) male mice. Our results revealed that normalization of the Dyrk1A copy number in TS mice improved working and reference memory based on the Morris water maze and contextual conditioning based on the fear conditioning test and rescued hippocampal LTP. Concomitant with these functional improvements, normalization of the Dyrk1A expression level in TS mice restored the proliferation and differentiation of hippocampal cells in the adult dentate gyrus (DG) and the density of GABAergic and glutamatergic synapse markers in the molecular layer of the hippocampus. However, normalization of the Dyrk1A gene dosage did not affect other structural (e.g., the density of mature hippocampal granule cells, the DG volume and the subgranular zone area) or behavioral (i.e., hyperactivity/attention) alterations found in the TS mouse. These results suggest that Dyrk1A overexpression is involved in some of the cognitive, electrophysiological and neuromorphological alterations, but not in the structural alterations found in DS, and suggest that pharmacological strategies targeting this gene may improve the treatment of DS-associated learning disabilities.
Data from: Metabolite profile of a mouse model of Charcot-Marie-Tooth type 2D neuropathy: implications for disease mechanisms and interventions
Charcot-Marie-Tooth disease encompasses a genetically heterogeneous class of heritable polyneuropathies that result in axonal degeneration in the peripheral nervous system. Charcot-Marie-Tooth type 2D neuropathy (CMT2D) is caused by dominant mutations in glycyl tRNA synthetase (GARS). Mutations in the mouse Gars gene result in a genetically and phenotypically valid animal model of CMT2D. How mutations in GARS lead to peripheral neuropathy remains controversial. To identify putative disease mechanisms, we compared metabolites isolated from the spinal cord of Gars mutant mice and their littermate controls. A profile of altered metabolites that distinguish the affected and unaffected tissue was determined. Ascorbic acid was decreased fourfold in the spinal cord of CMT2D mice, but was not altered in serum. Carnitine and its derivatives were also significantly reduced in spinal cord tissue of mutant mice, whereas glycine was elevated. Dietary supplementation with acetyl-L-carnitine improved gross motor performance of CMT2D mice, but neither acetyl-L-carnitine nor glycine supplementation altered the parameters directly assessing neuropathy. Other metabolite changes suggestive of liver and kidney dysfunction in the CMT2D mice were validated using clinical blood chemistry. These effects were not secondary to the neuromuscular phenotype, as determined by comparison with another, genetically unrelated mouse strain with similar neuromuscular dysfunction. However, these changes do not seem to be causative or consistent metabolites of CMT2D, because they were not observed in a second mouse Gars allele or in serum samples from CMT2D patients. Therefore, the metabolite 'fingerprint' we have identified for CMT2D improves our understanding of cellular biochemical changes associated with GARS mutations, but identification of efficacious treatment strategies and elucidation of the disease mechanism will require additional studies.
04/04 - Spatial and Amplitude Dynamics of Neurostimulation: Insights from the Acute Intrahippocampal Kainate Seizure Mouse Model
<p>Dataset #4 of 4</p>
02/04 - Spatial and Amplitude Dynamics of Neurostimulation: Insights from the Acute Intrahippocampal Kainate Seizure Mouse Model
<p>Dataset #2 of 4</p>
Single cell RNA-seq transcriptomic profile of circulating immune and progenitor cells in a mouse model of neonatal hypoxic/ischemic (HI) brain damage.
<p>Hematopoietic cells play a pivotal role in regulating the inflammatory and reparative immune responses triggered after ischemic tissue damage. The response initiated within the injured tissue leads to compositional and transcriptional changes in circulating hematopoietic and progenitor cells, which have been utilized as biomarkers. While the importance of different immune and progenitor cell subtypes in the development of ischemic damage has been extensively researched in adult tissue injuries, there has been limited investigation in neonates. This is a critical developmental stage where ischemic damage can result in severe and irreversible health consequences if not promptly treated. To determine how ischemic damage could affect circulating cells in neonates, we have induced hypoxic-ischemic (HI) brain damage in seven-day-old mice, characterized by focal white and gray-matter injury (Rice-Vannucci model). Brain damage and circulating cells were analyzed at 48h post-HI, the intermediate reparative/inflammatory response phase post-injury. We applied scRNAseq to dissect the transcriptional and cellular composition changes in the peripheral blood of HI-treated and SHAM control neonates. This study provides the first scRNAseq dataset for immune and progenitor circulating cells in newborns with cerebral HI damage. It may help to identify biomarkers and selective therapeutic approaches aimed at modulating inflammatory and reparative pathways. </p><p>CD1 postnatal day 7 (P7) mice were subjected to hypoxic/ischemic (HI) brain injury by permanent ligation of the left common carotid artery followed, after 2h recover, by relocation to a hypoxia chamber for 90 minutes. Sham control mice (SHAM) underwent a skin incision and wound closure followed by hypoxia exposure. Circulating blood cells were collected from SHAM and HI mice at P9. After red blood cells (RBC) lysis, 7AAD-Ter119- cells were FACS sorted and analysed using sc RNAseq. Other samples were FACS sorted for CD45+CD11+ and CD45-CD31+ cells and mixed.</p>
Figure 7 from: Almudaris SA, Gatea FK (2024) Effects of topical Ivermectin on imiquimod-induced Psoriasis in mouse model – Novel findings. Pharmacia 71: 1-14. https://doi.org/10.3897/pharmacia.71.e114753
Figure 7 Histopathological section of mice skin (clobetasol control group) showing hyperkeratosis (black arrow), absence of parakeratosis & Munro's abscess. And epidermal granular layer (yellow arrow) with mild acanthosis, mild papillary thinning, and few rete ridges (green arrow). The dermis shows mild lymphocytic infiltrate. H&E stain (4×,10×).
Figure 11 from: Almudaris SA, Gatea FK (2024) Effects of topical Ivermectin on imiquimod-induced Psoriasis in mouse model – Novel findings. Pharmacia 71: 1-14. https://doi.org/10.3897/pharmacia.71.e114753
Figure 11 Comparison between induced non-treated group and all induced treated groups regarding histopathological scores (Baker score) and observational score (PASI score).
Figure 4 from: Almudaris SA, Gatea FK (2024) Effects of topical Ivermectin on imiquimod-induced Psoriasis in mouse model – Novel findings. Pharmacia 71: 1-14. https://doi.org/10.3897/pharmacia.71.e114753
Figure 4 Histopathological section of mice skin (healthy control group) showing normal skin architecture including K = keratin, E = epidermis, D = dermis, AD = adnexa, S.C = subcutaneous tissue, M = muscles, B.V = blood vessels. H&E stain (4×,10×).
Figure 3 from: Almudaris SA, Gatea FK (2024) Effects of topical Ivermectin on imiquimod-induced Psoriasis in mouse model – Novel findings. Pharmacia 71: 1-14. https://doi.org/10.3897/pharmacia.71.e114753
Figure 3 Scoring for skin inflammation severity, the pictures show different inflammation levels of the dorsal skin on which the test substances were applied on day 8 of the Experiment. A. Represents the healthy group; B. Represents the IMQ-induced group; C. Represents the vehicle group; D. Represents Clobetasol treated group; E. Represents the Ivermectin treated group; F. Represents Ivermectin + Clobetasol treated group.
Figure 6 from: Almudaris SA, Gatea FK (2024) Effects of topical Ivermectin on imiquimod-induced Psoriasis in mouse model – Novel findings. Pharmacia 71: 1-14. https://doi.org/10.3897/pharmacia.71.e114753
Figure 6 Histopathological section of mice skin (vehicle group) showing hyperkeratosis, parakeratosis (black arrow), with focal neutrophilic infiltration (the Munro's abscess) in red arrow, with epidermal acanthosis and thinning papillae and elongated rete ridges (green arrow), and lack of granular layer. The dermis shows moderate to severe inflammatory lymphocytic infiltration (blue arrow). H&E stain (4×,10×).
Figure 9 from: Almudaris SA, Gatea FK (2024) Effects of topical Ivermectin on imiquimod-induced Psoriasis in mouse model – Novel findings. Pharmacia 71: 1-14. https://doi.org/10.3897/pharmacia.71.e114753
Figure 9 Histopathological section of mice skin (Ivermectin treatment group) showing mild keratosis (black arrow), with the absence of Munro's abscess and parakeratosis and epidermal mild acanthosis with few rete ridges and mild papillary thinning (green arrow). The dermis shows severe lymphocytic infiltrate. H&E stain (4×,10×).
Figure 2 from: Almudaris SA, Gatea FK (2024) Effects of topical Ivermectin on imiquimod-induced Psoriasis in mouse model – Novel findings. Pharmacia 71: 1-14. https://doi.org/10.3897/pharmacia.71.e114753
Figure 2 Induction of Psoriasis in mice. A Mouse before Induction. B Mouse after Induction by Imiquimod cream.
ScienceDex guides
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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.