We isolated and selected intestinal adenoma organoids from villin-CreER; Apcflox/flox and villin-CreER; Apcflox/flox; Prox1flox/flox mice and added tamoxifen to induce the deletion of the Apc and Prox1 genes in the intestinal epitheliul ex vivo. Microarray experiments were carried out 7 days after the addition of tamoxifen.
Prox1 promotes expansion of the colorectal cancer stem cell population to fuel tumor growth and ischemia resistance.
Specimen part
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Oncogenic mutations in intestinal adenomas regulate Bim-mediated apoptosis induced by TGF-β.
Specimen part, Treatment
View SamplesIntestinal crypts isolated from Apcflox/flox; villin-CreERT mice were treated with Tamoxifen to induce the deletion of Apc. Tamoxifen-treated organoids were selected in the absence of Wnt agonists and then treated with TGF-beta.
Oncogenic mutations in intestinal adenomas regulate Bim-mediated apoptosis induced by TGF-β.
Specimen part, Treatment
View SamplesHomeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxd4 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.
Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.
Specimen part
View SamplesHomeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxc8 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.
Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression.
Sex, Disease
View SamplesHere we exploit the essential process of Xchromosome dosage compensation to elucidate basic mechanisms that control the assembly, genomewide binding, and function of gene regulatory complexes that act over large chromosomal territories. We demonstrate that a subunit of C. elegans MLL/COMPASS, a gene-activation complex, acts within the dosage compensation complex (DCC), a condensin complex, to target the DCC to both X chromosomes of hermaphrodites and thereby reduce chromosome-wide gene expression. The DCC binds to two categories of sites on X: rex sites that recruit the DCC in an autonomous, sequence- dependent manner, and dox sites that reside primarily in promoters of expressed genes and bind the DCC robustly only when attached to X. We find that DCC mutants that abolish rex-site binding do not eliminate dox-site binding, but instead reduce it to the level observed at autosomal binding sites in wild-type animals. Changes in DCC binding to these non-rex sites occur throughout development and correlate with transcriptional activity of adjacent genes. Moreover, autosomal DCC binding is enhanced by rex-site binding in cis in X-autosome fusion chromosomes. Thus, dox and autosomal sites exhibit similar binding properties. Our data support a model for DCC binding in which low-level DCC binding at dox and autosomal sites is dictated by intrinsic properties correlated with high transcriptional activity. Sex-specific DCC recruitment to rex sites then greatly elevates DCC binding to dox sites in cis, which lack intrinsically high DCC affinity on their own. We also show here that the C. elegans DCC achieves dosage compensation through its effects on transcription.
An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression.
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View SamplesBarley cv. Morex inoculated with Fusarium graminearum (isolate Butte 86) or water (mock). Sampled at 24, 48, 72, 96 and 144 hours after treatment. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Jayanand Boddu. The equivalent experiment is BB9 at PLEXdb.]
Transcriptome analysis of the barley-Fusarium graminearum interaction.
Specimen part, Time
View SamplesAnalysis of the role of PARP1 in gene transcription in MCF7 cells under non-stress conditions. The hypothesis was that PARP1 activity in MCF7 cells plays a role in gene transcription. The results indicate that PARP1 inhibition does not significantly affect transcription after 6 hours of treatment.
Basal activity of a PARP1-NuA4 complex varies dramatically across cancer cell lines.
Specimen part, Cell line
View SamplesAnalysis of the role of PARP1 in gene transcription in cell lines with variable PARP1 activity.
Basal activity of a PARP1-NuA4 complex varies dramatically across cancer cell lines.
Specimen part, Cell line
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