This SuperSeries is composed of the SubSeries listed below.
Analyses of a Mutant Foxp3 Allele Reveal BATF as a Critical Transcription Factor in the Differentiation and Accumulation of Tissue Regulatory T Cells.
Specimen part
View SamplesFoxP3 is a central regulator of immunological tolerance, controlling the development and function of regulatory T (Treg) cells. To dissect the complex processes orchestrated by FoxP3, we investigated impacts of three autoimmune disease-associated missense FoxP3 mutations (i.e., I363V, A384T, R397W) through knock-in mutagenesis in mice.
Analyses of a Mutant Foxp3 Allele Reveal BATF as a Critical Transcription Factor in the Differentiation and Accumulation of Tissue Regulatory T Cells.
Specimen part
View SamplesFoxP3 is a central regulator of immunological tolerance, controlling the development and function of regulatory T (Treg) cells. To dissect the complex processes orchestrated by FoxP3, we investigated impacts of three autoimmune disease-associated missense FoxP3 mutations in mice.
Analyses of a Mutant Foxp3 Allele Reveal BATF as a Critical Transcription Factor in the Differentiation and Accumulation of Tissue Regulatory T Cells.
Specimen part
View SamplesFoxP3 is a central regulator of immunological tolerance, controlling the development and function of regulatory T (Treg) cells. To dissect the complex processes orchestrated by FoxP3, we investigated impacts of three autoimmune disease-associated missense FoxP3 mutations in mice. The I363V and R397W mutations were loss-of-function mutations, causing multi-organ inflammation by globally compromising Treg cell physiology. By contrast, the A384T mutation induced a distinctive tissue-restricted inflammation by specifically impairing the ability of Treg cells to compete with pathogenic T cells in certain non-lymphoid tissues.
Analyses of a Mutant Foxp3 Allele Reveal BATF as a Critical Transcription Factor in the Differentiation and Accumulation of Tissue Regulatory T Cells.
Specimen part
View SamplesVitamin A (VA) restriction for beef cattle improves meat marbling. However, its molecular mechanisms are not completely elucidated.
Microarray analysis of Longissimus thoracis muscle gene expressions in vitamin A-restricted Japanese Black steers in middle fattening stage.
Sex, Age, Specimen part
View SamplesBackground
Expression quantitative trait loci mapping identifies new genetic models of glutathione S-transferase variation.
No sample metadata fields
View SamplesMicroarray analysis of isolated lymphatic endothelial cells from cervical lymph nodes (CLNs) of ischemic mice showed the activation of transmembrane tyrosine kinase pathways.
Brain-to-cervical lymph node signaling after stroke.
Treatment
View SamplesXBP1 is a transcription factor that is induced by unconventional splicing associated with endoplasmic reticulum stress and plays a role in development of liver and plasma cells. We previously reported that brain derived neurotrophic factor (BDNF) leads to splicing of XBP1 mRNA in neurites, and that XBP1 is required for BDNF-induced neurite extension and branching. To search for the molecular mechanisms of how XBP1 plays a role in neural development, comprehensive gene expression analysis was performed in primary telencephalic neurons obtained from Xbp1 knockout mice at embryonic day 12.5. By searching for the genes induced by BDNF in wild type neurons but this induction was reduced in Xbp1 knockout mice, we found that upregulation of three GABAergic markers, somatostatin (Sst), neuropeptide Y (Npy), and calbindin (Calb1), were compromised in Xbp1 knockout neurons. Attenuated induction of Npy and Calb1 was confirmed by quantitative RT-PCR. In neurons lacking in Xbp1, upregulation of GABAergic markers was attenuated. Impaired BDNF-induced neurite extension in Xbp1 knockout neurons might be mediated by disturbed BDNF-induced differentiation of GABAergic interneurons.
Attenuated BDNF-induced upregulation of GABAergic markers in neurons lacking Xbp1.
Specimen part
View SamplesRationale: Obstructive sleep apnea (OSA) has been associated with metabolic dysregulation and systemic inflammation. This may be due to pathophysiologic effects of OSA on visceral adipose tissue. We sought to assess the transcriptional consequences of OSA on adipocytes by utilizing pathway-focused analyses.
A pathway-based analysis on the effects of obstructive sleep apnea in modulating visceral fat transcriptome.
Subject
View SamplesAeromonas caviae has been associated with human gastrointestinal disease. Strains of this species typically lack virulence factors (VFs) such as enterotoxins and hemolysins that are produced by other human pathogens of the Aeromonas genus. Microarray profiling of murine small intestinal extracts, 24 hours after oral infection with an A. caviae strain, provides evidence of a Th1 type immune response. A large number of gamma-interferon (-IFN) induced genes are up-regulated as well as several tumor necrosis factor-alpha (TNF-) transcripts. A. caviae has always been considered an opportunistic pathogen because it lacks obvious virulence factors. This current effort suggests A. caviae colonizes murine intestinal tract and causes what has been described by others as a dysregulatory cytokine response leading to an irritable bowel-like syndrome. This response would explain why a number of diarrheal waterborne outbreaks have been attributed to A. caviae even though it lacks obvious enteropathogenic properties.
Aeromonas caviae strain induces Th1 cytokine response in mouse intestinal tract.
No sample metadata fields
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