This SuperSeries is composed of the SubSeries listed below.
Systematic Functional Dissection of Common Genetic Variation Affecting Red Blood Cell Traits.
Specimen part, Cell line
View SamplesExpression analyses comparing c-Fos expressing keratinocytes vs non-expressing controls.
Inflammation-mediated skin tumorigenesis induced by epidermal c-Fos.
Specimen part, Treatment, Time
View SamplesAt 35 DAP whole kernels (pericarp + endosperm + embryo) without glumes of green house grown ears of heterozygous (+/bt2-H2328), self-pollinated plants were visually divided into pools of phenotypically normal looking kernels (small indentation, slightly smaller than mutant kernels, genotype +/+ or +/bt2-H2328) and pools of phenotypically mutant kernels (plump, round kernels, slightly larger than normal kernels, genotype bt2-H2328/bt2-H2328). Pools consisted of 4 kernels. 3 different ears were used for a biological duplicate.
Transcriptional and metabolic adjustments in ADP-glucose pyrophosphorylase-deficient bt2 maize kernels.
No sample metadata fields
View SamplesHexose-6-phosphate dehydrogenase (H6PD)is the initial component of a pentose phosphate pathway inside the endoplasmic reticulum (ER) that generates NADPH for ER enzymes. In liver, H6PD is required for the 11-oxoreductase activity of 11ss-hydroxysteroid dehydrogenase type 1 (11ss-HSD1), which converts inactive 11-oxo glucocorticoids to their active 11-hydroxyl counterparts; consequently, H6PD null mice are relatively insensitive to glucocorticoids, exhibiting fasting hypoglycemia, increased insulin sensitivity despite elevated circulating levels of corticosterone, and increased basal and insulin-stimulated glucose uptake in muscles normally enriched in Type II (fast) fibers which have increased glycogen content. They also display a progressive vacuolar myopathy evident after 4 weeks of age.
Deletion of hexose-6-phosphate dehydrogenase activates the unfolded protein response pathway and induces skeletal myopathy.
No sample metadata fields
View SamplesAging has been shown to be under genetic control in C. elegans. We performed Affymetrix micorarray-based transcriptional profililng of wild type C. elegans strain Bristol N2 during aging to detect temporal changes in gene expression.
A decline in p38 MAPK signaling underlies immunosenescence in Caenorhabditis elegans.
Specimen part
View SamplesSox3 has been shown to be expressed within neural progenitors of the developing mouse central nervous system. However, identification of Sox3 targets within neural progenitors has remained elusive.
Dbx1 is a direct target of SOX3 in the spinal cord.
Specimen part, Cell line
View SamplesThe oocytes found within the primordial follicles of mammalian ovaries remain quiescent for months to years until they receive the appropriate signals to undergo the primordial to primary follicle transition and initiate folliculogenesis. The molecular mechanisms and extracellular signaling factors that regulate this process remain to be fully elucidated. The current study investigates the mechanisms utilized by anti-Mllerian hormone (AMH; i.e. Mllerian inhibitory substance) to inhibit the primordial to primary follicle transition. Ovaries from 4-day-old rats were placed into organ culture and incubated in the absence or presence of AMH, either alone or in combination with known stimulators of follicle transition, including basic fibroblast growth factor (bFGF), kit ligand (KITL), or keratinocyte growth factor (KGF). Following 10 days of culture, the ovaries were sectioned, stained, and morphologically evaluated to determine the percentage of primordial versus developing follicles. As previously demonstrated, AMH treatment decreased primordial to primary follicle transition. Interestingly, AMH inhibited the stimulatory actions of KITL, bFGF, and KGF. Therefore, AMH can inhibit the basal and stimulated development of primordial follicles. To investigate the mechanism of AMH actions, the influence AMH has on the ovarian transcriptome was analyzed. AMH treatment when compared with controls was found to alter the expression of 707 genes. The overall effect of AMH exposure is to decrease the expression of stimulatory factors, increase the expression of inhibitory factors, and regulate cellular pathways (e.g. transforming growth factor beta signaling pathway) that result in the inhibition of primordial follicle development. Analysis of the regulatory factors and cellular pathways altered by AMH provides a better understanding of the molecular control of primordial follicle development.
Actions of anti-Mullerian hormone on the ovarian transcriptome to inhibit primordial to primary follicle transition.
No sample metadata fields
View SamplesTranscriptome analysis of mRNA samples from a cohort of mice with histopathologically diagnosed Undifferentiated Myeloid Leukemia.
Analyzing tumor heterogeneity and driver genes in single myeloid leukemia cells with SBCapSeq.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesMus musculus (house mouse) Myeloid Leukemia RNA-Seq
Analyzing tumor heterogeneity and driver genes in single myeloid leukemia cells with SBCapSeq.
No sample metadata fields
View SamplesDiet-induced obesity is characterized by macrophage (MF) infiltration and low-grade chronic inflammation in white adipose tissue (WAT) leading to insulin resistance. WAT MF are highly heterogeneous in their origin, patterns of gene expression and activities: unlike infiltrating monocyte-derived MF that promote inflammation and metabolic dysfunction, tissue-resident WAT MF originally described as ‘M2’ are phenotypically anti-inflammatory and counteract obesity and insulin resistance. Despite the critical role of the balance between these MF populations in metabolic homeostasis, the molecular mechanisms and key players that establish the resident MF transcription program are poorly understood. We recently reported that glucocorticoid receptor (GR)-interacting protein (GRIP)1 - a nuclear receptor coactivator - cooperates with GR to repress transcription of inflammatory genes. Here, using mice conditionally lacking GRIP1 in MF (cKO), we show that GRIP1 promotes MF polarization in response to IL4 (M2(IL4)) via a nuclear receptor-independent pathway by serving as a coactivator for Kruppel-like factor (KLF)4 – a critical driver of tissue MF differentiation. Interestingly, in vivo, GRIP1 cKO mice challenged with high-fat diet develop massive MF infiltration and chronic inflammation in WAT and liver, fatty livers, hyperglycemia, hyperinsulinemia and glucose intolerance consistent with metabolic syndrome phenotype. Together, our findings identify GRIP1 as a critical regulator of immunometabolism, which relies on distinct transcriptional mechanisms to coordinate the balance between MF populations in vivo thereby protecting mice from obesity-induced metabolic disease. Overall design: 1. Examination of IL4 induced transcriptome in in vitro differentiated primary bone marrow-derived macrophages. 2. Examination of macrophage transcriptome in macrophages isolated from the white adipose tissue of the WT and GRIP1(cKO) conditional KO animals
The transcriptional coregulator GRIP1 controls macrophage polarization and metabolic homeostasis.
Sex, Age, Specimen part, Subject
View Samples