Liver X Receptors (LXRa and ß) are ligand-activated transcription factors that play a key role in the control of lipid homeostasis, as well as modulation of immunity and inflammation. Besides ligand binding, LXR activity can be regulated by posttranslational modifications, such as phosphorylation. This study aims to assess changes in bone marrow derived macrophage transcriptional profiles of mice that carry LysMcre directed phosphorylation deficient-version of LXRa compared (S196A) to wild-type (WT). Overall design: BMDM mRNA profiles of either LdlrKO or M-LXRa-S196A-LdlrKO male mice after being fed a Western diet for 12 weeks. 12 samples, 4 groups, in triplicate: (1) LdlrKO basal, (2) LdlrKO+ ligand, (3) M-LXRa-S196A-LdlrKO basal, (4) M-LXRa-S196A-LdlrKO+ligand
Disrupting LXRα phosphorylation promotes FoxM1 expression and modulates atherosclerosis by inducing macrophage proliferation.
Specimen part, Cell line, Subject
View SamplesWe access the activity-dependent genes in olfactory neuron cells with unilateral naris occlusion model with mouse. Overall design: mRNA profile of olfactory epithelia between closed and open sides of mice naris was compared
Activity-Dependent Gene Expression in the Mammalian Olfactory Epithelium.
Specimen part, Cell line, Subject
View SamplesConditional deletion of Lhx2, and to a lesser extent, Emx2 in olfactory neurons alters odorant receptor expression frequency.
Lhx2 Determines Odorant Receptor Expression Frequency in Mature Olfactory Sensory Neurons.
Specimen part
View SamplesConditional deletion of Lhx2, and to a lesser extent, Emx2 in olfactory neurons alters odorant receptor expression frequency.
Lhx2 Determines Odorant Receptor Expression Frequency in Mature Olfactory Sensory Neurons.
Specimen part
View SamplesConditional deletion of Lhx2, and to a lesser extent, Emx2 in olfactory neurons alters odorant receptor expression frequency.
Lhx2 Determines Odorant Receptor Expression Frequency in Mature Olfactory Sensory Neurons.
Specimen part
View SamplesConditional deletion of Lhx2, and to a lesser extent, Emx2 in olfactory neurons alters odorant receptor expression frequency. This series describes 1 of the 5 array experiments.
Lhx2 Determines Odorant Receptor Expression Frequency in Mature Olfactory Sensory Neurons.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Lhx2 Determines Odorant Receptor Expression Frequency in Mature Olfactory Sensory Neurons.
Specimen part
View SamplesConditional deletion of Lhx2, and to a lesser extent, Emx2 in olfactory neurons alters odorant receptor expression frequency.
Lhx2 Determines Odorant Receptor Expression Frequency in Mature Olfactory Sensory Neurons.
Specimen part
View SamplesOdorants are thought to activate sets of odorant receptors in vivo, but capturing sets of responsive receptors in vivo has never been accomplished.
In vivo identification of eugenol-responsive and muscone-responsive mouse odorant receptors.
Specimen part
View SamplesHoxb8 mutant mice show compulsive behavior similar to trichotillomania, a human obsessive-compulsive-spectrum disorder. The only Hoxb8 lineage-labeled cells in the brains of mice are microglia, suggesting that defective Hoxb8 microglia caused the disorder. What is the source of the Hoxb8 microglia? It has been posited that all microglia progenitors arise at embryonic day (E) 7.5 during yolk sac hematopoiesis, and colonize the brain at E9.5. In contrast, we show the presence of two microglia subpopulations: canonical, non-Hoxb8 microglia and Hoxb8 microglia. Unlike non- Hoxb8 microglia, Hoxb8 microglia progenitors appear to be generated during the second wave of yolk sac hematopoiesis, then detected in the aorto-gonad-mesonephros (AGM) and fetal liver, where they are greatly expanded, prior to infiltrating the E12.5 brain. Further, we demonstrate that Hoxb8 hematopoietic progenitor cells taken from fetal liver are competent to give rise to microglia in vivo. Although the two microglial subpopulations are very similar molecularly, and in their response to brain injury and participation in synaptic pruning, they show distinct brain distributions which might contribute to pathological specificity. Non-Hoxb8 microglia significantly outnumber Hoxb8 microglia, but they cannot compensate for the loss of Hoxb8 function in Hoxb8 microglia, suggesting further crucial differences between the two subpopulations. Overall design: Green (non-Hoxb8, control) and yellow (Hoxb8, experimental) microglia data sets
Correction: Two distinct ontogenies confer heterogeneity to mouse brain microglia (doi: 10.1242/dev.152306).
Age, Specimen part, Cell line, Subject
View Samples