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ShareScore release 0.9.0
Dataset results
54 results for “Dystrophin”
In vivo genome editing restores dystrophin expression in Duchenne muscular dystrophy patient muscle fibers
GEO Series GSE168007. Homo sapiens. 118 samples. Type: Other; Expression profiling by high throughput sequencing.
Multi-level omics analysis of dystrophin loss and therapeutic restoration in a murine model
GEO Series GSE64420. Mus musculus; synthetic construct. 22 samples. Type: Expression profiling by array; Non-coding RNA profiling by array.
Histone deacetylase 4 represses dystrophin-glycoprotein (DGC) complex expression
GEO Series GSE10678. Mus musculus. 8 samples. Type: Expression profiling by array.
RNA sequencing of dystrophin- and utrophin-deficient HeLa cells reveals overlapping transcriptomic alterations
GEO Series GSE289357. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Full-length dystrophin restoration via targeted genomic integration by AAV-CRISPR in a humanized mouse model of Duchenne muscular dystrophy
GEO Series GSE173224. Mus musculus. 186 samples. Type: Other.
Dock3 is essential for normal myogenic fusion and alters dystrophin-deficiency pathologies
GEO Series GSE141621. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Long-term maintenance of dystrophin expression and resistance to injury of skeletal muscle in gene-edited mice
GEO Series GSE180771. Mus musculus. 24 samples. Type: Expression profiling by high throughput sequencing.
Dystrophin Deficiency Derives Phenotype Switching in Vascular Smooth Muscle Cells
GEO Series GSE232219. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Effect of the lack of dystrophin on the gene expression profile of hiPSC-derived cardiomyocytes
GEO Series GSE226170. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing.
Partial dataset related to the article: "Fibrosis Rescue Improves Cardiac Function in Dystrophin-Deficient Mice and Duchenne Patient-Specific Cardiomyocytes by Immunoproteasome Modulation".
<p>This record contains raw data related to the article: "Fibrosis Rescue Improves Cardiac Function in Dystrophin-Deficient Mice and Duchenne Patient-Specific Cardiomyocytes by Immunoproteasome Modulation".</p> <p>Abstract</p> <p>Patients affected by Duchenne muscular dystrophy (DMD) develop a progressive dilated cardiomyopathy<br> characterized by inflammatory cell infiltration, necrosis, and cardiac fibrosis. Standard<br> treatments consider the use of b-blockers and angiotensin-converting enzyme inhibitors that are<br> symptomatic and unspecific toward DMD disease. Medications that target DMD cardiac fibrosis are<br> in the early stages of development. We found immunoproteasome dysregulation in affected hearts<br> of mdx mice (murine animal model of DMD) and cardiomyocytes derived from induced pluripotent<br> stem cells of patients with DMD. Interestingly, immunoproteasome inhibition ameliorated cardiomyopathy<br> in mdx mice and reduced the development of cardiac fibrosis. Establishing the<br> immunoproteasome inhibitionedependent cardioprotective role suggests the possibility of modulating<br> the immunoproteasome as new and clinically relevant treatment to rescue dilated cardiomyopathy<br> in patients with DMD.</p>
RNA sequencing of HSkM myotubes deficient in DMD, full-length dystrophin (DP427) and utrophin reveals common transcriptomic alterations
GEO Series GSE303672. Homo sapiens. 15 samples. Type: Expression profiling by high throughput sequencing.
A novel CRISPR-Cas9 strategy to target DYSTROPHIN mutations downstream of exon 44 in patient-specific DMD iPSCs
GEO Series GSE262976. Homo sapiens. 15 samples. Type: Expression profiling by high throughput sequencing.
Dataset related to the article "Establishment of a Duchenne muscular dystrophy patient-derived induced pluripotent stem cell line carrying a deletion of exons 51–53 of the dystrophin gene (CCMi003-A) "
<p>This record contains raw data related to the article: "Establishment of a Duchenne muscular dystrophy patient-derived induced pluripotent stem cell line carrying a deletion of exons 51–53 of the dystrophin gene (CCMi003-A) "</p> <p>Abstract:</p> <p>Duchenne's muscular dystrophy (DMD) is a neuromuscular disorder affecting skeletal and cardiac muscle function, caused by mutations in the dystrophin (DMD) gene. Dermal fibroblasts, isolated from a DMD patient with a reported deletion of exons 51 to 53 in the DMD gene, were reprogramed into induced pluripotent stem cells (iPSCs) by electroporation with episomal vectors containing the reprograming factors: OCT4, SOX2, LIN28, KLF4, and L-MYC. The obtained iPSC line showed iPSC morphology, expression of pluripotency markers, possessed trilineage differentiation potential and was karyotypically normal.</p>
Dataset related to the article "Multiomic Approaches to Uncover the Complexities of Dystrophin-Associated Cardiomyopathy"
<p>This record contains raw data related to the article “Multiomic Approaches to Uncover the Complexities of Dystrophin-Associated Cardiomyopathy”</p> <p>Despite major progress in treating skeletal muscle disease associated with dystrophinopathies, cardiomyopathy is emerging as a major cause of death in people carrying dystrophin gene mutations that remain without a targeted cure even with new treatment directions and advances in modelling abilities. The reasons for the stunted progress in ameliorating dystrophin-associated cardiomyopathy (DAC) can be explained by the difficulties in detecting pathophysiological mechanisms which can also be efficiently targeted within the heart in the widest patient population. New perspectives are clearly required to effectively address the unanswered questions concerning the identification of authentic and effectual readouts of DAC occurrence and severity. A potential way forward to achieve further therapy breakthroughs lies in combining multiomic analysis with advanced preclinical precision<br> models. This review presents the fundamental discoveries made using relevant models of DAC and how omics approaches have been incorporated to date.</p>
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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.