Introduction of brain tumor-relevant genetic aberrations initiates different subtypes of brain tumor-like neoplasms in cerebral organoids Overall design: Comparison of abundances (TPM) from different brain tumor organoid groups
Author Correction: Genetically engineered cerebral organoids model brain tumor formation.
Specimen part, Subject
View SamplesIntroduction of brain tumor-relevant genetic aberrations initiates different subtypes of brain tumor-like neoplasms in cerebral organoids Overall design: Comparison of transcriptomes from different brain tumor organoid groups
Author Correction: Genetically engineered cerebral organoids model brain tumor formation.
Specimen part, Subject
View SamplesEffect of LUBEL catalytic dead mutation in immune response Overall design: Mutation was introduced in the LUBEL catalytic region by CRISPR/Cas9 techonology in Drosophila melanogaster and their transcriptome was compared in control (sample 23930 to 23941) and e.coli pricked samples (sample 28984 to 28995).
Linear ubiquitination by LUBEL has a role in Drosophila heat stress response.
Sex, Specimen part, Subject
View SamplesEffect of LUBEL catalytic dead mutation upon Heastshock Overall design: Mutation was introduced in CG11321 catalytic region by CRISPR/Cas9 techonology in Drosophila melanogaster and transcriptome was compared in untreated and heatshocked samples
Linear ubiquitination by LUBEL has a role in Drosophila heat stress response.
Treatment, Subject
View SamplesWe describe a critical role for Cdk6 in JAK2V617F+ MPN evolution. The absence of Cdk6 ameliorates clinical symptoms and prolongs survival of JAK2V617F fl/+ vav-Cre mice. The Cdk6 protein interferes with three hallmarks of disease: besides regulating malignant stem cell quiescence, it promotes NFkB signaling and contributes to cytokine production while inhibiting apoptosis. The treatment with palbociclib did not mirror these effects, showing that the functions of Cdk6 in MPN pathogenesis are largely kinase-independent. Overall design: LSK-sorted (FACS) bone marrow cells from 8-week-old VavCre;Jak2+/+; Cdk6+/+, VavCre;Jak2V617F; Cdk6+/+, VavCre;Jak2V617F; Cdk6-/-, VavCre; Jak2+/+; Cdk6-/- mice, and the same cell type from palbociclib-treated (38mg/kg, 3x in one week) VavCre;Jak2V617F; Cdk6+/+ mice, n=3 for all genotypes
CDK6 coordinates <i>JAK2</i> <sup><i>V617F</i></sup> mutant MPN via NF-κB and apoptotic networks.
Specimen part, Treatment, Subject
View SamplesFirst, transcriptome analysis of purified CD31+ endothelial cells (ECs) from VEGF-treated sprouting embryoid bodies showed angiogenesis as the top affected category when Apelin is not present. In addition, loss of Apelin resulted in the modulation of pathways in ECs related to vasculogenesis, cell adhesion and response to hypoxia. Ingenuity Pathway Analysis (IPA) further identified VEGFR pathway as the main upstream regulator affected in endothelial cells, closely followed by the TGFß1 and TNF pathways, all reduced in the absence of Apelin. The most inhibited genes from the VEGFR pathway in the absence of Apelin are angiogenesis-related genes. Second, transcriptome analysis of CD31+/CD105+ ECs sorted from Apelin wild-type and Apln-depleted tumors found a significant decrease in processes associated with endothelial cell proliferation and angiogenesis in ECs sorted out of Apelin-depleted tumors using IPA. Further, IPA predicted a decrease in the adhesion of granulocytes and upstream regulator analysis showed that proteins of the TGF-superfamily, Inhibin-ßA and TGF-ß1, as well as C/EBP-alpha, ß-Catenin, ErbB2 and EGFR are predicted to be inhibited upstream regulators in ECs isolated from Apelin-depleted tumors. Overall design: Transcriptome analysis of purified CD31+ endothelial cells from VEGF-treated in vitro sprouting vessels in Apelin presence or absence. Transcriptome analysis of tumor endothelial cells from Apelin wild-type and depleted conditions. We report the application of Smart-Seq2 sequencing to populations of 100 endothelial cells, sorted from tumors that were Apelin wild-type or depleted.
Apelin inhibition prevents resistance and metastasis associated with anti-angiogenic therapy.
Sex, Specimen part, Cell line, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.
Specimen part
View SamplesIndicated cells were subjected to RNAi against linker histone H1, Nautilus (control), or GFP (control). RNA was isolated and subjected to Affymetrix GeneChIP Drosophila Genome 2.0 arrays
Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.
Specimen part
View SamplesSalivary glands or larval ovaries were isolated from transgenic flies expressing RNAi targeting Nautilus (control) or linker histone H1 using a Tub-Gal4 driver. Overall design: ~200 larvae were used to isolate salivary glands or ovaries, independently. Total RNA was isolated using Trizol reagent following manufacturer''s guidelines. Then 5 µg of total RNA was separated on a polyacrylamide gel, and 18-29 nt small RNAs were isolated for cloning.
Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.
Specimen part, Subject
View SamplesCotton fiber were used for the expression analysis at different developmental stages
Transcriptome dynamics during fibre development in contrasting genotypes of Gossypium hirsutum L.
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