Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA277714 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Medulloblastoma (MB) is the most common malignant primary pediatric brain tumor and is currently divided into 4 subtypes based on different genomic alterations, gene expression profiles and response to treatment: WNT, Sonic Hedgehog (SHH), Group 3 and Group 4. The extensive heterogeneity has made it difficult to assess the relevance of genes to malignant progression. For example, expression of the transcription factor, OTX2, is frequently dysregulated in multiple MB variants; however, it's role may be subtype specific. Here, we utilized human embryonic stem cell-derived neural precursors to determine the role of OTX2 in MB tumor progression using gain and loss of function studies. We used global gene expression profiling to determine what transcripts and pathways were differentially expressed following knockdown of OTX2 in transformed or neoplastic human embryonic neural precursor cells. OTX2 was knocked down in transformed human embyronic neural precursors (trans-hEN) using Silencer select siRNAs. trans-hEN OTX2 KD and scrambled control trans-hENs were then grown as neurospheres in defined medium and collected at passage 1. RNA was extracted using the Norgen All-in-One kit.
2015-08-25 | E-GEOD-66671 | biostudies-arrayexpress
Project description:Medulloblastoma (MB) is the most common malignant primary pediatric brain tumor and is currently divided into 4 subtypes based on different genomic alterations, gene expression profiles and response to treatment: WNT, Sonic Hedgehog (SHH), Group 3 and Group 4. The extensive heterogeneity has made it difficult to assess the relevance of genes to malignant progression. For example, expression of the transcription factor, OTX2, is frequently dysregulated in multiple MB variants; however, it's role may be subtype specific. Here, we utilized human embryonic stem cell-derived neural precursors to determine the role of OTX2 in MB tumor progression using gain and loss of function studies. We used global gene expression profiling to determine what transcripts and pathways were differentially expressed following knockdown of OTX2 in transformed or neoplastic human embryonic neural precursor cells.
2015-08-25 | GSE66671 | GEO
Project description:Expression data comparing OTX2-overexpressing human neural precursors to human neural precursor cells
| PRJNA277713 | ENA
Project description:Medulloblastoma (MB) is the most common malignant primary pediatric brain tumor and is currently divided into 4 subtypes based on different genomic alterations, gene expression profiles and response to treatment: WNT, Sonic Hedgehog (SHH), Group 3 and Group 4. The extensive heterogeneity has made it difficult to assess the relevance of genes to malignant progression. For example, expression of the transcription factor, OTX2, is frequently dysregulated in multiple MB variants; however, it's role may be subtype specific. Here, we utilized human embryonic stem cell-derived neural precursors to determine the role of OTX2 in MB tumor progression using gain and loss of function studies. We used global gene expression profiling to determine what transcripts and pathways were differentially expressed following overexpression of OTX2 in human embryonic neural precursor cells. OTX2 was stably overexpressed in human embyronic neural precursors (hEN) by lentiviral transduction. OTX2-hENs and control hENs were then grown as neurospheres in defined medium and collected at passage 2. RNA was extracted using the Norgen All-in-One kit.
2015-08-25 | E-GEOD-66670 | biostudies-arrayexpress
Project description:Medulloblastoma (MB) is the most common malignant primary pediatric brain tumor and is currently divided into 4 subtypes based on different genomic alterations, gene expression profiles and response to treatment: WNT, Sonic Hedgehog (SHH), Group 3 and Group 4. The extensive heterogeneity has made it difficult to assess the relevance of genes to malignant progression. For example, expression of the transcription factor, OTX2, is frequently dysregulated in multiple MB variants; however, it's role may be subtype specific. Here, we utilized human embryonic stem cell-derived neural precursors to determine the role of OTX2 in MB tumor progression using gain and loss of function studies. We used global gene expression profiling to determine what transcripts and pathways were differentially expressed following overexpression of OTX2 in human embryonic neural precursor cells.
2015-08-25 | GSE66670 | GEO
Project description:We report that the cell of origin plays an important role in this metastatic tropism. Following injection into the arterial circulation of mice, each of the identically transformed cell types gave rise to different metastatic patterns. Using gene expression analysis, we identified the chemokine receptor CXCR4 as being instrumental in determining the distinct metastatic patterns between skeletal muscle precursor cells and skeletal myoblasts. 3 independent cell lines of primary human skeletal myoblasts, primary skeletal muscle cell precursors, and each of these cell lines transformed with hTERT, the early region of SV40 encoding T-Ag and t-Ag, and RasG12V analysis of primary human skeletal myoblasts, primary skeletal muscle cell precursors, and each of these cell lines transformed with hTERT, the early region of SV40 encoding T-Ag and t-Ag, and RasG12V
2016-02-13 | E-GEOD-19294 | biostudies-arrayexpress
Project description:Ankrd11 is a potential chromatin regulator implicated in neural development and autism spectrum disorder (ASD) with no known function in the brain. Here, we show that knockdown of Ankrd11 in developing murine or human cortical neural precursors caused decreased proliferation, reduced neurogenesis, and aberrant neuronal positioning. Similar cellular phenotypes and aberrant ASD-like behaviors were observed in Yoda mice carrying a point mutation in the Ankrd11 HDAC-binding domain. Consistent with a role for Ankrd11 in histone acetylation, Ankrd11 was associated with chromatin, colocalized with HDAC3, and expression and histone acetylation of Ankrd11 target genes were altered in Yoda neural precursors. Moreover, the Ankrd11 knockdown-mediated decrease in precursor proliferation was rescued by inhibiting histone acetyltransferase activity or expressing HDAC3. Thus, Ankrd11 is a crucial epigenetic regulator of neural development that controls histone acetylation and gene expression, thereby providing a likely explanation for its association with cognitive dysfunction and ASD. We used microarrays to compare the gene expression profile in embryonic neurospheres prepared from neocortices of WT and Ankrd11Yod/+ mice E14.5 cortical secondary neurosheres 5 days post-passage were collected and total RNA extracted. cDNA was hybridized on Affymetrix Mouse Gene 2.0 ST Array and gene expression was analyzed using Parterk software. In total, 6 Ankrd11Yod/+ and 5 WT embryos were used.
2014-11-15 | E-GEOD-63303 | biostudies-arrayexpress
Project description:Here, we have addressed the mechanisms that determine genesis of the correct numbers of neurons during development, focusing upon the embryonic cortex. We identify in neural precursors a repressive complex involving eIF4E1 and its binding partner 4E-T that coordinately represses translation of proteins that determine neurogenesis. This eIF4E1/4E-T complex is present in granules with the processing body proteins Lsm1 and Rck, and disruption of this complex causes premature and enhanced neurogenesis and neural precursor depletion. Analysis of the 4E-T complex shows that it is highly enriched in mRNAs encoding transcription factors and differentiation-related proteins. These include the proneurogenic bHLH mRNAs, which colocalize with 4E-T in granules, and whose protein products are aberrantly upregulated following knockdown of eIF4E, 4E-T, or processing body proteins. Thus, neural precursors are transcriptionally primed to generate neurons, but an eIF4E/4E-T complex sequesters and represses translation of proneurogenic proteins to determine appropriate neurogenesis. We obtained 3 biological replicates of IgG-bound RNA, 4E-T-bound RNA, and cooresponding total RNA input from mouse E12-13 cortices. RNA samples were analyzed on the Affymetrix Mouse Gene 2.0 ST Arrays.
2014-09-25 | E-GEOD-61729 | biostudies-arrayexpress
Project description:Here, we have addressed the mechanisms that determine genesis of the correct numbers of neurons during development, focusing upon the embryonic cortex. We identify in neural precursors a repressive complex involving eIF4E1 and its binding partner 4E-T that coordinately represses translation of proteins that determine neurogenesis. This eIF4E1/4E-T complex is present in granules with the processing body proteins Lsm1 and Rck, and disruption of this complex causes premature and enhanced neurogenesis and neural precursor depletion. Analysis of the 4E-T complex shows that it is highly enriched in mRNAs encoding transcription factors and differentiation-related proteins. These include the proneurogenic bHLH mRNAs, which colocalize with 4E-T in granules, and whose protein products are aberrantly upregulated following knockdown of eIF4E, 4E-T, or processing body proteins. Thus, neural precursors are transcriptionally primed to generate neurons, but an eIF4E/4E-T complex sequesters and represses translation of proneurogenic proteins to determine appropriate neurogenesis.
2014-09-25 | GSE61729 | GEO
Project description:Despite the history of Otx2 research over three decades, the role of Otx2 expressed in the brain-forming anterior epiblast during gastrulation stages has not been clarified. We paid attention to the fact epiblast regions exist where Otx2 expression is absent or downregulated, namely the posterior epiblast and tissue belts along the neural plate bending. Developmental events that follow filling these expression gaps with exogenous Otx2 expression would be informative concerning the roles of Otx2 during gastrulation. The effects were pleiotropic: (1) Development of open and flat midbrain and hindbrain, which occurred via unzippering of once closed neural tube; (2) Precocious neural tube development at the cervical level that gave rise to thick and unclosed neural tissue; (3) The absence of the sinus rhomboidalis where NMP stem cells multiply to provide a cell source for the trunk posterior extension, resulting in the trunk posterior extension; (4) Inhibition of somite development. To elucidate principles underlying these developmental abnormalities, the cellular events were analyzed using live imaging of epiblasts, cell states were characterized via transcriptome analysis, and spatial organization of transcription factor expression was determined by immunohistology. Common denominating Otx2 activities that account for these pleiotropic effects were identified: (1) Significant boosts of neuroepithelium development, which even overrides the bipotential nature of NMPs, resulting in the loss of paraxial mesoderm precursor and loss of multiplying NMP stem cell population, and (2) The development of bending-refractory neural tissues. By virtue of these Otx2 functions, Otx2-expressing anterior epiblasts develop into the vast brain tissue in advance of the trunk neurogenesis that occurs in much smaller scale. We did not observe the exogenous Otx2 expression affecting the CNS regional specification.
2025-04-26 | GSE292068 | GEO