Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA268529 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Evolutionary changes in promoter and enhancer activity during corticogenesis (non-human)
| PRJNA259649 | ENA
Project description:<p>We used epigenetic profiling to map active enhancers in the developing human limb and cortex as described in two published studies: <ul> <li>Cotney J, Leng J, Yin J, Reilly SK et al. The evolution of lineage-specific regulatory activities in the human embryonic limb. <a href="https://www.ncbi.nlm.nih.gov/pubmed/23827682">Cell 2013</a>;154(1):185-96. </li> <li>Reilly SK, Yin J, Ayoub AE, Emera D et al. Evolutionary changes in promoter and enhancer activity during human corticogenesis. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25745175">Science 2015</a>;347(6226):1155-9.</li> </ul> </p> <p> We also used ChIP-seq to map binding sites for the chromatin modifier <a href="https://www.ncbi.nlm.nih.gov/gene/?term=CHD8"><i>CHD8</i></a> in the developing human brain, as described in one published study: <ul> <li>Cotney J, Muhle RA, Sanders SJ, Liu L et al. The autism-associated chromatin modifier <a href="https://www.ncbi.nlm.nih.gov/gene/?term=CHD8"><i>CHD8</i></a> regulates other autism risk genes during human neurodevelopment. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25752243">Nat Commun 2015</a>;6:6404.</li> </ul> </p> <p> We are also depositing primary human sequence reads related to processed datasets in the Gene Expression Omnibus under the following accession numbers: <a href="https://www.ncbi.nlm.nih.gov/gds/?term=GSE42413">GSE42413</a> (Cotney et al. <a href="https://www.ncbi.nlm.nih.gov/pubmed/23827682">2013</a>); <a href="https://www.ncbi.nlm.nih.gov/gds/?term=GSE63649">GSE63649</a> (Reilly et al. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25745175">2015</a>); <a href="https://www.ncbi.nlm.nih.gov/gds/?term=GSE57369">GSE57369</a> (Cotney et al. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25752243">2015</a>). </p>
| phs001226 | dbGaP
Project description:Evolutionary changes in gene regulation during cortical development likely contributed to the expansion and specialization of the cortex in humans. However, the lack of a regulatory map of the human embryonic cortex has hindered identification of these changes and the biological processes they influenced. We performed genome-wide epigenetic profiling to compare promoter and enhancer activity during corticogenesis in human, rhesus, and mouse. We identified 2,855 promoters and 8,996 enhancers that have gained activity in human based on increased epigenetic marking. To detect biological pathways enriched for these changes, we mapped promoters and enhancers exhibiting epigenetic gains onto modules of co-expressed genes constructed using spatio-temporally rich expression data from developing human cortex. We identified multiple modules enriched in human lineage epigenetic gains. Gains in enriched modules were associated with genes functioning in neuronal proliferation and migration, cortical patterning, and the extracellular matrix. Gain-enriched modules also showed correlated gene expression patterns and similar transcription factor binding site enrichments in promoters and enhancers, suggesting they are connected by common regulatory mechanisms. Our results reveal coordinated patterns of potential regulatory changes associated with conserved developmental processes in corticogenesis, providing insight into human cortical evolution.
2015-03-06 | GSE63648 | GEO
Project description:Single-nucleus RNA sequencing (snRNA-seq) was used to profile the transcriptome of 16,015 nuclei in human adult testis. This dataset includes five samples from two different individuals. This dataset is part of a larger evolutionary study of adult testis at the single-nucleus level (97,521 single-nuclei in total) across mammals including 10 representatives of the three main mammalian lineages: human, chimpanzee, bonobo, gorilla, gibbon, rhesus macaque, marmoset, mouse (placental mammals); grey short-tailed opossum (marsupials); and platypus (egg-laying monotremes). Corresponding data were generated for a bird (red junglefowl, the progenitor of domestic chicken), to be used as an evolutionary outgroup.
2021-11-08 | E-MTAB-11063 | biostudies-arrayexpress
Project description:Evolutionary changes in gene regulation during cortical development likely contributed to the expansion and specialization of the cortex. However, the lack of a regulatory map of the embryonic cortex has hindered identification of these changes and the biological processes they influenced. We performed genome-wide epigenetic profiling to compare promoter and enhancer activity during corticogenesis in rhesus and mouse. We identified 2,855 promoters and 8,996 enhancers that have gained activity in based on increased epigenetic marking. To detect biological pathways enriched for these changes, we mapped promoters and enhancers exhibiting epigenetic gains onto modules of co-expressed genes constructed using spatio-temporally rich expression data from developing cortex. We identified multiple modules enriched in lineage epigenetic gains. Gains in enriched modules were associated with genes functioning in neuronal proliferation and migration, cortical patterning, and the extracellular matrix. Gain-enriched modules also showed correlated gene expression patterns and similar transcription factor binding site enrichments in promoters and enhancers, suggesting they are connected by common regulatory mechanisms. Our results reveal coordinated patterns of potential regulatory changes associated with conserved developmental processes in corticogenesis, providing insight into cortical evolution.
2015-03-06 | GSE60838 | GEO
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression. Two-condition experiment, Normoxic MSCs vs. Hypoxic MSCs.
2011-02-19 | E-GEOD-20463 | biostudies-arrayexpress
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.
2014-12-02 | GSE63741 | GEO