Gene expression profile of LysMCre/Cre and KLF2/ primary peritoneal macrophages following 6 hours of LPS treatment.
The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.
Age, Specimen part
View SamplesWe 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.
No sample metadata fields
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.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
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 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
View SamplesOver expression of recombinant proteins is known to cause a metabolic burden to the host cells which leads to down regulation of both growth rates and protein expression. Most studies in this regard have been conducted in low density shake flask cultures which does not capture the essential features of an industrial scale bioprocess. In the present work we studied the transcriptomic profiling at different specific growth rates while expressing the recombinant human interferon beta in fed batch cultures with complex media. These conditions mimicked the industrial fermentations for recombinant proteins.
Comparative transcriptomic profile analysis of fed-batch cultures expressing different recombinant proteins in Escherichia coli.
No sample metadata fields
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