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2,168 results for “deletion”
Novel DMD mouse model carrying a multi-exonic Dmd deletion exhibit progressive muscular dystrophy and early-onset cardiomyopathy
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Data from: Two genes, one culprit - a functional candidate validation of a <em>SPATA7</em> deletion in dogs with day blindness/retinal degeneration
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Mature mRNA processing that deletes 3′ end sequences directs translational activation and embryonic development
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A point mutation and large deletion at the candidate avirulence locus AvrMlp7 in the poplar rust fungus correlate with poplar RMlp7 resistance breakdown
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Data from: A SACS deletion variant in Great Pyrenees dogs causes autosomal recessive neuronal degeneration
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Data from: HIF prolyl hydroxylase 2/3 deletion disrupts astrocytic integrity and exacerbates neuroinflammation
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Data from: Major group-B enterovirus populations deleted in the noncoding 5' region of genomic RNA modulate activation of the type I interferon pathway in cardiomyocytes and induce myocarditis
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ARPIP: Ancestral sequence Reconstruction with insertions and deletions under the Poisson Indel Process
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GTPBP2 in-frame deletion in a canine model with progressive retinal degeneration
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Filename (1 files) Size Progress Delete Appendix 2 CD013203
<p>This is a table for Cochrane review: Best LMJ, Leung J, Freeman SC, Sutton AJ, Cooper NJ, Milne EJ, Cowlin M, Payne A, Walshaw D, Thorburn D, Pavlov CS, Davidson BR, Tsochatzis E, Williams NR, Gurusamy KS. Induction immunosuppression in adults undergoing liver transplantation: a network meta-analysis. Cochrane Database of Systematic Reviews 2018, Issue 11. Art. No.: CD013203.</p>
Prostate-specific deletion of Cdh1 induces murine prostatic inflammation and bladder overactivity
<p>Benign Prostatic Hyperplasia (BPH) is an age-related debilitating prostatic disease that is frequently associated with prostatic inflammation and bothersome lower urinary tract symptoms (LUTS). Animal models have shown that formalin- and bacterial-induced prostatic inflammation can induce bladder dysfunction; however, the underlying mechanisms contributing to prostatic inflammation in BPH and bladder dysfunction are not clear. We previously reported that E-cadherin expression in BPH is down-regulated in hyperplastic nodules compared to expression in adjacent normal tissues. Here, we explored the potential consequences of prostatic E-cadherin down-regulation on the prostate and bladder <i>in vivo</i> using an inducible murine model of prostate luminal epithelial-specific deletion of <i>Cdh1</i>. The PSA-CreER<sup>T2</sup> transgenic mouse strain expressing tamoxifen-inducible CreER<sup>T2</sup> recombinase driven by a 6-kb human PSA promoter/enhancer was crossed with the B6.129-<i>Cdh1</i><sup>tm2Kem</sup>/J mouse to generate bigenic PSA-CreER<sup>T2</sup>/<i>Cdh1</i><sup>-/-</sup> mice. Deletion of E-cadherin was induced by transient administration of tamoxifen when mice reached sexual maturity (7 weeks of age). At 21-23 weeks of age, the prostate, bladder, and prostatic urethra were examined histologically, and bladder function was assessed using Void Spot Assays and cystometry. Mice with <i>Cdh1</i> deletion had increased prostatic epithelial hyperplasia, inflammation, and stromal changes at 21-23 weeks of age, as well as changes in bladder voiding function compared to age-matched controls. Thus, loss of E-cadherin in the murine prostate could result in prostatic defects that are characteristic of BPH and lower urinary tract symptoms, suggesting that E-cadherin down-regulation could be a driving force in human BPH development and progression.</p>
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live cell super-resolution data_dual_color_cell_line_SCR_deletion
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live cell super-resolution data_dual_color_cell_line_E15_deletion
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Identification of a novel non-coding deletion in Allan-Herndon-Dudley syndrome by long-read HiFi genome sequencing
<p>These are the VCF files of structural variant (SV) calls for two sibling patients (II:2 [GMPB009_1] and II:3 [GMPB009_4]) generated by PacBio HiFi long-read genome sequencing.</p> <p>Sequence reads were processed using the <a href="https://github.com/PacificBiosciences/pb-human-wgs-workflow-snakemake">PacBio Human WGS workflow</a> with the human reference genome (hg38), and SVs were identified using '<a href="https://github.com/PacificBiosciences/svpack">svpack</a>'.</p>
Early onset of adult deafness in the Rhodesian Ridgeback is associated with in-frame deletion in the EPS8L2 gene
<p>Domestic dogs exhibit diverse types of both congenital and non-congenital hearing losses. Rhodesian Ridgebacks can suffer from a progressive hearing loss in the early stage of their life, a condition known as early onset of adult deafness (EOAD), where they lose their hearing ability within 1-2 years after birth. In order to investigate the genetic basis of this hereditary hearing disorders, we performed a genome-wide association study (GWAS) by using a sample of 23 affected and 162 control Rhodesian Ridgebacks. We identified a genomic region on canine chromosome 18 (CFA18) that is strongly associated with EOAD, and our subsequent targeted Sanger sequencing analysis identified a 12-bp inframe deletion in EPS8L2 (CFA18:25,868,739-25,868,751 in the UMICH_Zoey_3.1/canFam5 reference genome build). Additional genotyping confirmed a strong association between the 12-bp deletion and EOAD, where all affected dogs were homozygous for the deletion, while none of the control dogs was a deletion homozygote. A segregation pattern of this deletion in a 2-generation nuclear family indicated an autosomal recessive mode of inheritance. Since EPS8L2 plays a critical role in the maintenance and integrity of the inner ear hair cells in humans and other mammals, the inframe deletion found in this study represents a strong candidate causal mutation for EOAD in Rhodesian Ridgebacks. Genetic and clinical similarities between childhood deafness in humans and EOAD in Rhodesian Ridgebacks emphasizes the potential value of this dog breed in translational research in hereditary hearing disorders.</p>
ENDOG_NGS data related to article "Biallelic variants in ENDOG associated with mitochondrial myopathy and multiple mtDNA deletions" submitted to Cells
<p>vcf file of the targeted NGS; csv of the top 50 rare variants from WES prioritized by eVAI software; csv of WES rare variants prioritized by eVAI software using patient's phenotype information.</p>
NOTICE OF THE DELETION OF UNPUBLISHED ARTICLE: Competence, Leadership Skills, and Professional Commitment of Elementary Teachers in the National Capital Region
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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.
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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.