Time course micro array experiment to identify transcriptional changes in response to exposure of hFLs to different combinations of small molecules during direct neuronal reprogramming
Small molecules increase direct neural conversion of human fibroblasts.
Specimen part, Treatment, Time
View SamplesTranscriptomic studies revealed that hundreds of mRNAs show differential expression in the brains of sleeping versus awake rats, mice, flies, and sparrows. Although these results have offered clues regarding the molecular consequences of sleep and sleep loss, their functional significance thus far has been limited. This is because the previous studies pooled transcripts from all brain cells, including neurons and glia.
Effects of sleep and wake on oligodendrocytes and their precursors.
Specimen part
View SamplesAlthough recent studies support regenerative potential based on cardiac progenitor cells (CPCs), it remains unclear what cues regulate CPC fate. Using 2- and 3D-culture models, we demonstrate that the two most abundantly expressed matrix proteins in the heart, laminin and fibronectin, have opposite roles in CPC fate decision. CPCs on fibronectin showed predominantly nuclear localization of the transcriptional co-activator YAP and maintained proliferation. In contrast, seeding on laminin induced cytosolic retention and degradation of YAP and altered gene expression, which preceded decreased proliferation and enhanced lineage commitment. RNA-sequencing identified Plk2 as candidate target gene of YAP. Plk2 expression depended on YAP stability, was rapidly downregulated on laminin, and its regulation was sufficient to rescue and/or mimic the CPC response to laminin and fibronectin, respectively. These findings propose a novel role of Plk2 and identify an early molecular mechanism in matrix-instructed CPC fate with potential implications for therapeutic cardiac regeneration. Overall design: Expression profiling of cardiac progenitor cells in suspension and cultured on dishes coated with laminin or fibronectin or on non-coated dishes (biological triplicates each)
Polo-Like Kinase 2 is Dynamically Regulated to Coordinate Proliferation and Early Lineage Specification Downstream of Yes-Associated Protein 1 in Cardiac Progenitor Cells.
No sample metadata fields
View SamplesPaired-end sequencing of Vector and H-Ras expressing cell lines: p53-del and WT-p53 We found that activated forms of H-Ras and PIK3CA oncogene lead to repression of p63, a p53 family member. They also lead to induction of EMT, a cancer-related process. Our results suggest that, through Ras regulation of p63, this oncogene can drive mammary epithelial cells towards greater invasive ability. Overall design: 4 samples analyzed with 3 replicates each, control samples for each H-Ras line are the Vector cell line created at the same time
Repression of p63 and induction of EMT by mutant Ras in mammary epithelial cells.
Cell line, Subject
View SamplesThe intermediate filament protein Nestin serves as a biomarker for stem cells and has been used to identify subsets of cancer stem-like cells. However, the mechanistic contributions of Nestin to cancer pathogenesis are not understood. Here we report that Nestin binds the hedgehog pathway transcription factor Gli3 to mediate the development of medulloblastomas of the hedgehog subtype. In a mouse model system, Nestin levels increased progressively during medulloblastoma formation resulting in enhanced tumor growth. Conversely, loss of Nestin dramatically inhibited proliferation and promoted differentiation. Mechanistic investigations revealed that the tumor-promoting effects of Nestin were mediated by binding to Gli3, a zinc finger transcription factor that negatively regulates hedgehog signaling. Nestin binding to Gli3 blocked Gli3 phosphorylation and its subsequent proteolytic processing, thereby abrogating its ability to negatively regulate the hedgehog pathway. Our findings show how Nestin drives hedgehog pathway-driven cancers and uncover in Gli3 a therapeutic target to treat these malignancies.
Nestin Mediates Hedgehog Pathway Tumorigenesis.
Specimen part
View SamplesComparison between cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel
Exon array analyses across the NCI-60 reveal potential regulation of TOP1 by transcription pausing at guanosine quartets in the first intron.
Sex, Age, Specimen part, Cell line
View SamplesComparison between cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel.
Topoisomerase I levels in the NCI-60 cancer cell line panel determined by validated ELISA and microarray analysis and correlation with indenoisoquinoline sensitivity.
Sex, Age, Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Homer1a is a core brain molecular correlate of sleep loss.
No sample metadata fields
View SamplesThese studies adress differential changes in gene expression between sleep deprived and control mice. We profiled gene expression at four time points across the 24H Light/Dark cycle to take into account circadian influences and used three different inbred strains to understand the influence of genetic background.
Homer1a is a core brain molecular correlate of sleep loss.
No sample metadata fields
View SamplesThese studies adress differential changes in gene expression between 6h sleep deprived and control mice in the brain and the liver. We profiled gene expression in three different inbred strains to understand the influence of genetic background.
Homer1a is a core brain molecular correlate of sleep loss.
No sample metadata fields
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