Microarray was used to delineate the global gene expression profile underlying the specific developmental program of two divergent antigen-specific T helper subsets (Th22 versus Th17) by identifying upregulation or downregulation of key lineage-determining transcription factors, cytokines, chemokines and other genes that govern their functional attributes.
Th22 cells are an important source of IL-22 for host protection against enteropathogenic bacteria.
Specimen part
View SamplesMAP kinases are integral to the mechanisms by which cells respond to a wide variety of environmental stresses. In Caenorhabditis elegans, the KGB-1 JNK signaling pathway regulates the response to heavy metal stress. The deletion mutants of this cascade show hypersensitivity to heavy metals like copper or cadmium. However, factors that function downstream of KGB-1 pathway are not well characterized.
The Caenorhabditis elegans JNK signaling pathway activates expression of stress response genes by derepressing the Fos/HDAC repressor complex.
Age
View SamplesInvestigating the effects of two different classes of KDM1A inhibitors on the transcriptome of AML cell lines Overall design: 16 different samples with biological replicates. Treatment for 24 and 72 hours with an irreversible KDM1A inhibitor (RN-1) or a reversible KDM1A inhibitor (GSK690) or an inactive isomer of the latter (GSK690*).
Pharmacological Inhibition of the Histone Lysine Demethylase KDM1A Suppresses the Growth of Multiple Acute Myeloid Leukemia Subtypes.
No sample metadata fields
View SamplesSmall molecule inhibitors of the bromodomain and extraterminal (BET) family of proteins are in clinical trials for a variety of cancers, but patient selection strategies are limited. This is due in part to the heterogeneity of response following BET inhibition (BETi), which includes differentiation, senescence, and cell death in subsets of cancer cell lines. To elucidate the dominant features defining response to BETi, we carried out phenotypic and gene expression analysis of both treatment naïve cell lines and engineered tolerant lines. We found that both de novo and acquired tolerance to BET inhibition are driven by the robustness of the apoptotic response and that genetic or pharmacological manipulation of the apoptotic signaling network can modify the phenotypic response to BETi. We further identify that ordered expression of the apoptotic genes BCL2, BCL2L1, and BAD significantly predicts response to BETi. Our findings highlight the role of the apoptotic network in response to BETi, providing a molecular basis for patient stratification and combination therapies. Overall design: Gene expression profiling of A375 melanoma cells or NOMO-1 AML cells treated with DMSO or the BET inhibitor, CPI203. Also, gene expression profiling of the respective derived BETi-tolerant cells treated with DMSO or CPI203.
Preclinical Anticancer Efficacy of BET Bromodomain Inhibitors Is Determined by the Apoptotic Response.
No sample metadata fields
View SamplesRecent studies indicated that the differentiation tendency of pluripotent stem cells (PSCs) was affected by a certain small molecule treatment. We found the combination of small molecules that bringed out the differentiation potentials of PSCs, and defined such state of PSC as CTraS.
Escape from Pluripotency via Inhibition of TGF-β/BMP and Activation of Wnt Signaling Accelerates Differentiation and Aging in hPSC Progeny Cells.
Specimen part, Subject
View SamplesThe mammalian forebrain is a tissue of stunning complexity comprised of numerous regions each containing many distinct cell types that differ in their intrinsic and synaptic physiology, morphology and connectivity. These differences are likely conferred by differential gene expression, but the extent and nature of cell type specific gene expression is largely unknown. Here, we carried out microarray analysis of twelve major classes of fluorescently labelled neurons within the forebrain and provide the first comprehensive view of gene expression differences. The results demonstrate a profound molecular heterogeneity among neuronal subtypes, represented disproportionately by gene paralogs, and begin to reveal the genetic programs underlying the fundamental divisions between neuronal classes including that between glutamatergic and GABAergic neurons.
Molecular taxonomy of major neuronal classes in the adult mouse forebrain.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.
Age, Specimen part, Treatment
View SamplesSmall RNA-seq on MCF10A, HCT116 and HCT116p53-/- cell lines after induction of DNA damage (5 Gy Irradiation). Overall design: Small RNA-seq on MCF10A, HCT116 and HCT116p53-/- at 4 and 24 hours after induction of DNA damage (5 Gy Irradiation), done in duplicate with respective control (0 hour) using illumina Genome Analyzer IIx
p53 shapes genome-wide and cell type-specific changes in microRNA expression during the human DNA damage response.
Cell line, Treatment, Subject, Time
View SamplesAnalysis of brown adipose tissue from Yin Yang 1 (YY1) brown fat specific knockout mice fed a high fat diet for 3 months. YY1 deficiency in brown adipose tissue leads to strong thermogenic deficiency. The goal was to identify the genes controlled by YY1 responsible of brown fat defective function.
Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.
Age, Specimen part, Treatment
View SamplesAnalysis of visceral white adipose tissue (EWAT) from Yin Yang 1 adipose-specific knockout mice exposed to cold (4C) for 4 days.
Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity.
Age, Specimen part, Treatment
View Samples