We measured gene expression in the adrenal glands of the Spontaneously Hypertensive Rat (SHR) and Wistar-Kyoto rat (WKY) using Affymetrix RG-U34A GeneChips. All rats were aged-matched at 4-weeks. The rats were obtained from the colonies at the Univeristy of California San Diego, La Jolla, CA.
Common genetic mechanisms of blood pressure elevation in two independent rodent models of human essential hypertension.
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View SamplesWe performed Affymetrix MG-U74Av2 GeneChip experiements on mRNA from the adrenal glands of the BPH hypertensive and BPL hypotensive mouse strains. All mice were aged-matched at 5 weeks. We obtained the mice from Jackson Laboratories, Bar Harbor, ME.
Neuroendocrine transcriptome in genetic hypertension: multiple changes in diverse adrenal physiological systems.
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Global metabolic consequences of the chromogranin A-null model of hypertension: transcriptomic detection, pathway identification, and experimental verification.
Sex, Specimen part
View SamplesThe objective of the experiment is to determine the genes differentially expressed in the liver of the chromogranin A knockout mouse (Mahapatra et al., 2005).
Global metabolic consequences of the chromogranin A-null model of hypertension: transcriptomic detection, pathway identification, and experimental verification.
Sex, Specimen part
View SamplesThe objective of the experiment is to determine the genes differentially expressed in the adrenal gland of the chromogranin A knockout mouse (Mahapatra et al., 2005).
Global metabolic consequences of the chromogranin A-null model of hypertension: transcriptomic detection, pathway identification, and experimental verification.
Sex, Specimen part
View SamplesThe expression level of a gene is often used as a proxy for determining whether the protein or RNA product is functional in a cell or tissue. Therefore, it is of fundamental importance to understand the global distribution of gene expression levels, and to be able to interpret it mechanistically and functionally. Here we use RNA sequencing of mouse Th2 cells, coupled with a range of other techniques, to show that all genes can be separated, based on their expression abundance, into two distinct groups: one group comprising of lowly expressed and putatively non-functional mRNAs, and the other of highly expressed mRNAs with active chromatin marks at their promoters. Similar observations are made in other data sets, including sources such as Drosophila. Overall design: RNA-seq data of two biological replicates of murine Th2 cells.
Single-cell RNA sequencing reveals T helper cells synthesizing steroids de novo to contribute to immune homeostasis.
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View SamplesWe performed RNA-seq to profile gene expression in the heads and whole bodies of 32 isofemale fly lines from two divergent microclimates at ''Evolution Canyon'' in Israel (16 fly lines from each microclimate). We also measured RNA editing levels in the head tissue of these flies. Overall design: For each of the 32 isofemale fly lines from ''Evolution Canyon'', gene expression profiles of whole bodies and heads, along with RNA editing profiles of heads of 3-5 day old male flies through RNA-seq.
Regulation of gene expression and RNA editing in Drosophila adapting to divergent microclimates.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Microcephaly gene links trithorax and REST/NRSF to control neural stem cell proliferation and differentiation.
Time
View SamplesThe progression from stem cell to differentiated neuron is associated with extensive chromatin remodeling that controls gene expression, but the mechanisms that connect chromatin to gene expression are not well defined. Here we show that mutation of ZNF335 causes severe human microcephaly ("small brain"), small somatic size, and neonatal death. Germline Znf335 null mutations are embryonically lethal in mice, whereas RNA-interference studies and postmortem human studies show that Znf335 is essential for neural progenitor self-renewal, neurogenesis, and neuronal differentiation. Znf335 is a component of a vertebrate-specific, trithorax H3K4 methylation complex, while global ChIP-seq and mRNA expression studies show that Znf335 is a previously unsuspected, direct regulator of REST/NRSF, a master regulator of neural gene expression and neural cell fate, as well as other essential neural-specific genes. Our results reveal ZNF335 as an essential link between H3K4 complexes and REST/NRSF, and provide the first direct evidence that this pathway regulates human neurogenesis and neuronal differentiation.
Microcephaly gene links trithorax and REST/NRSF to control neural stem cell proliferation and differentiation.
Time
View SamplesNeuropsychiatric consequences of poorly controlled seizures that begin in childhood can be devastating. School failure or behavioral difficulty in a child with epilepsy is common and can become the focus of concern for families. Current antiepileptic drugs compound problems with their CNS side effects; effective therapy is currently limited as little is known about the cellular and molecular changes caused by seizures in the developing brain. This study will investigate transcriptional regulation induced by early-life seizures and explore alternative nonpharmacological therapeutic strategies in reversing damages of early-life seizures. We will study the therapeutic efficacy of environmental enrichment in reducing seizure-induced neuronal injury and in modifying gene expression alterations. We will explore molecular mechanisms underlying the beneficial effects of enriched environment and examine how different genes act in concert to influence the outcome of seizure-induced damage.
Environmental enrichment reverses the impaired exploratory behavior and altered gene expression induced by early-life seizures.
No sample metadata fields
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