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GSE110308
Mus musculus
13 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We report transcriptional characterization of skeletal muscle macrophage subsets in normal and injured muscle after intramuscular injection with cardiotoxin. We profiled transcriptional differences in macrophage subsets from mice depleted of Treg cells using Foxp3-DTR mice. We uncovered an IFN-g-centered regulatory loop, in which Treg cells inhibit NK and T cells to control macrophage accumulation and phenotype during muscle regeneration.
Publication Title
T<sub>reg</sub> cells limit IFN-γ production to control macrophage accrual and phenotype during skeletal muscle regeneration.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Oryza sativa indica group
- 12 Downloadable Samples
- Affymetrix Rice Genome Array (rice)
Description
Potassium is one of the essential macronutrients required for plant growth and development. It plays a major role in different physiological processes like cell elongation, stomatal movement, turgor regulation, osmotic adjustment, and signal transduction by acting as a major osmolyte and component of the ionic environment in the cytosol and subcellular organelles.
Publication Title
Gene expression analysis of rice seedling under potassium deprivation reveals major changes in metabolism and signaling components.
Sample Metadata Fields
Specimen part, Treatment, Time
View Samples- Mus musculus
- 8 Downloadable Samples
Illumina HiSeq 2500
Description
We report age-related gene expression of Treg cells isolated from injured muscle and spleen. Male C57BL/6 Foxp3-GFP reporter mice were injured intramuscularly with cardiotoxin. Tregs were sorted directly into Trizol from injured muscle and spleen 4 days post-injury. Overall design: Gene expression profiling of muscle and splenic Tregs from 2- vs >6-month old mice (biological duplicate for each).
Publication Title
Poor Repair of Skeletal Muscle in Aging Mice Reflects a Defect in Local, Interleukin-33-Dependent Accumulation of Regulatory T Cells.
Sample Metadata Fields
Sex, Age, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2500
Description
We report gene expression of Treg cells isolated from injured muscle in IL-33 vs PBS treated mice. Male Foxp3-GFP C57BL/6 reporter (2 months old) mice were injured intramuscularly with cardiotoxin/rIL-33 (0.3 ug/muscle). Tregs were sorted directly into Trizol from injured muscle 4 days post-injury. Overall design: Gene expression profiling of muscle Tregs from IL-33 vs PBS injured mice.
Publication Title
Poor Repair of Skeletal Muscle in Aging Mice Reflects a Defect in Local, Interleukin-33-Dependent Accumulation of Regulatory T Cells.
Sample Metadata Fields
Sex, Age, Treatment, Subject
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Illumina Genome Analyzer IIx
Description
The Drosophila midgut is an ideal model system to study molecular mechanisms that interfere with the intestinal stem cells’ (ISCs) ability to function in tissue homeostasis. Due to the lack of a combination of molecular markers suitable to isolate ISCs from aged intestines, it has been a major challenge to study endogenous molecular changes of ISCs during aging. Our FACS-based approach using the esg-GAL4, UAS-GFP fly line allowed the isolation of a cell population enriched for ISCs from young and old midguts by their small size, little granularity and low GFP intensity. The isolated ISCs were subsequently used for RNA sequencing to identify endogenous changes in the transcriptome of young versus old ISCs. Overall design: Cell populations enriched for ISCs isolated from young (6-8 days old) and old (59-65 days old) midguts were sorted. Cells from three different batches of young and old midguts were subjected to Next Generation Sequencing using Illumina Genome Analyzer IIx.
Publication Title
Nipped-A regulates intestinal stem cell proliferation in <i>Drosophila</i>.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina Genome Analyzer
Description
Natural killer (NK) cells play a critical role in early host defense to infected and transformed cells. Here we show that mice deficient in Eri1, a conserved 3’-to-5’ exoribonuclease that represses RNA interference, have a cell-intrinsic defect in NK cell development and maturation. Eri1–/– NK cells displayed delayed acquisition of Ly49 receptors in the bone marrow and a selective reduction in Ly49D and Ly49H activating receptors in the periphery. Eri1 was required for immune-mediated control of mouse cytomegalovirus (MCMV) infection. Ly49H+ NK cells deficient in Eri1 failed to expand efficiently during MCMV infection, and virus-specific responses were also diminished among Eri1–/– T cells. We identified miRNAs as the major endogenous small RNA target of Eri1 in mouse lymphocytes. Both NK and T cells deficient in Eri1 displayed a global, sequence-independent increase in miRNA abundance. Ectopic Eri1 expression rescued defective miRNA expression in mature Eri1–/– T cells. Thus, mouse Eri1 regulates miRNA homeostasis in lymphocytes and is required for normal NK cell development and anti-viral immunity. Overall design: Small RNA profiling from wildtype and Eri1-deficient mouse CD4+ T cells
Publication Title
Eri1 regulates microRNA homeostasis and mouse lymphocyte development and antiviral function.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Interleukin 9 (IL-9) producing helper T (Th9) cells play a crucial role in allergic inflammation, autoimmunity, immunity to extracellular pathogens and anti-tumor immune response. In addition to Th9, Th2, Th17 and Foxp3+ Treg cells produce IL-9. Transcription factor that is critical for IL-9 induction in Th2, Th9 and Th17 cells has not been identified. Here we show that Foxo1, a forkhead family transcription factor, requires for IL-9 induction in Th9 and Th17 cells. We further show that inhibition of AKT enhances IL-9 induction in Th9 cells while it reciprocally regulates IL-9 and IL-17 in Th17 cells via Foxo1. Mechanistically, Foxo1 binds and transactivates IL-9 and IRF4 promoters in Th9, Th17 and iTregs. Furthermore, loss of Foxo1 attenuates IL-9 in mouse and human Th9 and Th17 cells, and ameliorates allergic inflammation in asthma. Our findings thus identify that Foxo1 is essential for IL-9 induction in Th9 and Th17 cells. Overall design: Transcriptional analysis of Th0 and TGF-beta 1 + IL-4 induced Th9 cells
Publication Title
Transcription factor Foxo1 is essential for IL-9 induction in T helper cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Knockout of G protein β5 impairs brain development and causes multiple neurologic abnormalities in mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Gb5 is a divergent, evolutionarily-conserved, member of the heterotrimeric G protein b subunit family that is expressed principally in brain and neuronal tissue. Among Gb isoforms, Gb5 is unique in its ability to heterodimerize with members of the R7 subfamily of the regulator of G protein signaling (RGS) proteins that contain G protein-g like (GGL) domains. Previous studies employing Gb5 knockout mice have shown that Gb5 is an essential stabilizer of GGL domain-containing RGS proteins and regulates the deactivation of retinal phototransduction and the proper functioning of retinal bipolar cells. The purpose of this study is to better understand the functions of Gb5 in the brain outside the visual system by employing molecular biology, immunohistochemistry and confocal imaging technologies. We show here that mice lacking Gb5 have a markedly abnormal neurologic phenotype that includes neurobehavioral developmental delay, wide-based gait, motor learning and coordination deficiencies, and hyperactivity. Using immunohistochemical analysis and a green fluorescent reporter of Purkinje cell maturation we show that the phenotype of Gb5-deficient mice includes, in part, delayed development of the cerebellar cortex, an abnormality that likely contributes to the neurobehavioral phenotype. Multiple neuronally-expressed genes are dysregulated in non-cerebellar portion of Gb5 KO mice.
Publication Title
Knockout of G protein β5 impairs brain development and causes multiple neurologic abnormalities in mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Gb5 is a divergent, evolutionarily-conserved, member of the heterotrimeric G protein b subunit family that is expressed principally in brain and neuronal tissue. Among Gb isoforms, Gb5 is unique in its ability to heterodimerize with members of the R7 subfamily of the regulator of G protein signaling (RGS) proteins that contain G protein-g like (GGL) domains. Previous studies employing Gb5 knockout mice have shown that Gb5 is an essential stabilizer of GGL domain-containing RGS proteins and regulates the deactivation of retinal phototransduction and the proper functioning of retinal bipolar cells. The purpose of this study is to better understand the functions of Gb5 in the brain outside the visual system by employing molecular biology, immunohistochemistry and confocal imaging technologies. We show here that mice lacking Gb5 have a markedly abnormal neurologic phenotype that includes neurobehavioral developmental delay, wide-based gait, motor learning and coordination deficiencies, and hyperactivity. Using immunohistochemical analysis and a green fluorescent reporter of Purkinje cell maturation we show that the phenotype of Gb5-deficient mice includes, in part, delayed development of the cerebellar cortex, an abnormality that likely contributes to the neurobehavioral phenotype. Multiple neuronally-expressed genes are dysregulated in cerebellum of Gb5 KO mice.
Publication Title
Knockout of G protein β5 impairs brain development and causes multiple neurologic abnormalities in mice.
Sample Metadata Fields
Specimen part
View Samples