14-3-3 proteins facilitate cytoplasmic-nuclear shuttling of transcription factors.Adipocyte differentiation requires the function of critical transcription factors to drive the development of a mature adipocyte. The aim of the study was to investigate if 14-3-3? is required for the adipogenic transcriptional program. Overall design: Examination of the transcriptome in siCon- and si14-3-3?-transfected 3T3-L1 cells undergoing differentiation at t=0, 24, and 48 hours.
14-3-3ζ coordinates adipogenesis of visceral fat.
No sample metadata fields
View SamplesDue to inherent differences in adipcoyte size between wildtype and knockout animals, we sought to examine if the decrease in adipocyte size was due to differences in the transcriptome and more specifcially, adipogenic genes. Overall design: Examination of the transcriptome in wildtype (WT) and knockout (KO) gonadal white adipose tissue from adult mice
14-3-3ζ coordinates adipogenesis of visceral fat.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Activation of GCN2 kinase by ribosome stalling links translation elongation with translation initiation.
Age
View SamplesRibosome stalling during translation has recently been shown to cause neurodegeneration, yet the signaling pathways triggered by stalled elongation complexes are unknown. To investigate these pathways we analyzed the brain of B6J-nmf205-/- mice in which neuronal elongation complexes are stalled at AGA codons due to deficiencies in a tRNA Arg(UCU) tRNA and GTPBP2, a mammalian ribosome rescue factor. Increased levels of phosphorylation of eIF2 (Ser51) were detected prior to neurodegeneration in these mice and transcriptome analysis demonstrated activation of ATF4, a key transcription factor in the integrated stress response (ISR) pathway. Genetic experiments showed that this pathway was activated by the eIF2 kinase, GCN2, in an apparent deacylated tRNA-independent fashion. Further we found that the ISR attenuates neurodegeneration in B6J-nmf205-/- mice, underscoring the importance of cellular and stress context on the outcome of activation of this pathway. These results demonstrate the critical interplay between translation elongation and initiation in regulating neuron survival during cellular stress.
Activation of GCN2 kinase by ribosome stalling links translation elongation with translation initiation.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Malignant catarrhal fever of cattle is associated with low abundance of IL-2 transcript and a predominantly latent profile of ovine herpesvirus 2 gene expression.
No sample metadata fields
View SamplesWe hypothesized that the relative abundances of host cell transcripts in lymph nodes of animals with malignant catarrhal fever (MCF), compared to healthy controls, may be used to identify pathways that may help to explain the pathogenesis of MCF. Therefore, an abundance of host cell gene expression patterns in lymph nodes of animals with MCF and healthy controls were analyzed by microarray. Indeed, a vast number of genes related to inflammatory processes, lymphocyte activation, cell proliferation and apoptosis were detected at different abundances. However, the IL-2 transcript was eminent among the transcripts, which were, compared to healthy controls, less abundant in animals with MCF. Compared to healthy cattle, bovines with MCF appear to mimic an IL-2 knockout phenotype that has been described in mice. This supports the hypothesis that immunopathogenic events are linked to the pathogenesis of MCF. IL-2-deficiency may play an important role in the process.
Malignant catarrhal fever of cattle is associated with low abundance of IL-2 transcript and a predominantly latent profile of ovine herpesvirus 2 gene expression.
No sample metadata fields
View SamplesMHCaCre induced knockout of Fog2flox.
Fog2 is critical for cardiac function and maintenance of coronary vasculature in the adult mouse heart.
Sex, Specimen part, Treatment
View SamplesPreterm birth is an important unsolved clinical problem. Despite advanced treatments, infants who survive prematurity remain at increased risk for permanent disabilities. In approximately one-third of cases, prematurity is related to infection and/or inflammation, which renders hostile the normally receptive intrauterine environment. Proinflammatory cytokines provoke up-regulation of genes that promote uterine contractions. Using monolayer cultures of human decidual cells as a model, we profiled the global pattern of gene expression in response to cytokine challenge.
Inflammatory gene networks in term human decidual cells define a potential signature for cytokine-mediated parturition.
Specimen part, Time
View SamplesPremature birth continues to be a challenging pregnancy complication, and a body of literature indicates that inflammation can contribute to premature delivery by converting a receptive uterine environment to a hostile one. Cytokines have been demonstrated to provoke up-regulation of inflammatory genes (e.g. interleukin-1, 6, and 8, tumor necrosis factor-alpha, cyclooxygenase-2, and microsomal prostaglandin E synthase-1).
Inflammatory gene regulatory networks in amnion cells following cytokine stimulation: translational systems approach to modeling human parturition.
Specimen part, Time
View SamplesSeveral studies have shown that bone mineral density (BMD), a clinically measurable predictor of osteoporotic fracture, is the sum of genetic and environmental influences. In addition, serum IGF-1 levels have been correlated to both BMD and fracture risk. We previously identified a Quantitative Trait Locus (QTL) for Bone Mineral Density (BMD) on mouse Chromosome (Chr) 6 that overlaps a QTL for serum IGF-1. The B6.C3H-6T (6T) congenic mouse is homozygous for C57BL/6J (B6) alleles across the genome except for a 30 cM region on Chr 6 that is homozygous for C3H/HeJ (C3H) alleles. This mouse was created to study biology behind both the BMD and the serum IGF-1 QTLs and to identify the gene(s) underlying these QTLs. Female 6T mice have lower BMD and lower serum IGF-1 levels at all ages measured. As the liver is the major source of serum IGF-1, we examined differential expression in the livers of fasted female B6 and 6T mice by microarray.
A chromosomal inversion within a quantitative trait locus has a major effect on adipogenesis and osteoblastogenesis.
No sample metadata fields
View Samples