This SuperSeries is composed of the SubSeries listed below.
Mapping gene regulatory circuitry of Pax6 during neurogenesis.
Specimen part
View SamplesPax6 is a highly conserved transcription factor among vertebrates and is important in various aspects of the central nervous system (CNS) development. However, the gene regulatory circuitry of Pax6 underlying these functions remains elusive. We find that, following expression in neural progenitor cells, Pax6 targets many promoters embedded in an active chromatin environment. Intriguingly, many of these sites are also bound by another progenitor factor, Sox2, which cooperates with Pax6 in gene regulation. A combinatorial analysis of Pax6 binding dataset with transcriptome changes in Pax6-deficient neural progenitors reveals a dual role for Pax6, in which it activates the neuronal (ectodermal) genes while concurrently represses the mesodermal and endodermal genes thereby ensuring the unidirectionality of lineage commitment towards glutamatergic neuronal differentiation. Furthermore, Pax6 is critical for inducing activity of transcription factors that elicit neurogenesis and repress others that promote non-neuronal lineages. In addition to many established downstream effectors, Pax6 directly binds and activates a number of genes that are specifically expressed in neural progenitors but have not been previously implicated in neurogenesis. The in utero knockdown of one such gene, Ift74, during brain development impairs polarity and migration of new-born neurons. These findings demonstrate new aspects of the gene regulatory circuitry of Pax6, revealing how it functions to control neuronal development at multiple levels to ensure unidirectionality and proper execution of the neurogenic program.
Mapping gene regulatory circuitry of Pax6 during neurogenesis.
Specimen part
View SamplesExpression profiling after Sox4 knockdown (KD) during epithelial to mesenchymal transition (EMT) in NMuMG reveals a significant number of genes that are transcriptionally deregulated.
Sox4 is a master regulator of epithelial-mesenchymal transition by controlling Ezh2 expression and epigenetic reprogramming.
Cell line, Treatment
View Sampleswe analyzed the gene expression profiles of Mat-Lylu cell lines (in duplicate) compared to G cell lines (in duplicate) using Affymetrix tools and dChip software. The objective was to find metastasis-associated genes in prostate cancer, using this in vitro model.
DNA microarray analysis reveals metastasis-associated genes in rat prostate cancer cell lines.
No sample metadata fields
View SamplesTo understand the global view of dysregulated genes and pathwyas in CRYAAN101D lenses, RNA sequencing of 2 & 4 months old CRYAAWT and CRYAAN101D lenses was carried out. Overall design: Determination of differential gene expression between CRYAAWT and CRYAAN101D in 2 & 4 months old lenses
Molecular mechanism of formation of cortical opacity in CRYAAN101D transgenic mice.
No sample metadata fields
View SamplesThiazolidinediones increase tissue insulin sensitivity and are protective against worsening of nephropathy and hypertension in diabetes. Mechanisms underlying protection at the renal level likely involve a variety of unknown changes in gene expression. We examined kidney gene expression in obese and lean Zucker rats in response to rosiglitazone (Avandia), a peroxisome proliferator activated receptor (gamma-subtype) agonist. Lean and obese Zucker rats were treated with either control chow or chow with added rosiglitazone (3 mg/kgbw) for 12 weeks (n = 3/group). Total kidney mRNA expression was evaluated using the Affymetrix Rat Genome 230 2.0 GeneChip. 903 probe sets were significantly (P < 0.05) altered with at least 1.5-fold changes between groups. In untreated obese rats, 300 probe sets were increased and 244 decreased, relative to lean. Increased genes included the -subunit of the epithelial sodium channel (ENaC), the thiazide-sensitive Na-Cl cotransporter, and aquaporin 3. Decreased genes included angiotensin converting enzyme, type 1 (ACE1). FatiGO analysis showed that the highest number of altered genes between lean and obese belonged to the categories: ion binding, hydrolase activity, and protein binding. RGZ increased expression of uncoupling protein 1 (UCP1), CD36, and fatty acid binding protein 4 (FAbp4) in both lean and obese rats. In obese rats, 33 genes were normalized by RGZ (no longer different from lean) including ACE1, fatty acid synthase (Fasn), and stearoyl-coenzyme A desaturase 2 (Scd2). Ingenuity Pathways System analysis of genes upregulated by RGZ in obese rats revealed two major nodes affected: PPAR-gamma and tumor necrosis factor alpha (TNF-alpha).
Chronic rosiglitazone therapy normalizes expression of ACE1, SCD1 and other genes in the kidney of obese Zucker rats as determined by microarray analysis.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A chromatin-modifying function of JNK during stem cell differentiation.
Specimen part, Treatment
View SamplesExpression profiling of from DMSO and SP600125 treated glutamatergic neurons reveals JNK target genes that are transcriptionally regulated by JNK signaling.
A chromatin-modifying function of JNK during stem cell differentiation.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
MicroRNAs reprogram normal fibroblasts into cancer-associated fibroblasts in ovarian cancer.
Specimen part, Time
View SamplesCampare the difference between pairwise NOF and coCAF tissues for three patients
MicroRNAs reprogram normal fibroblasts into cancer-associated fibroblasts in ovarian cancer.
Specimen part, Time
View Samples