Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126977 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Coactivator associated arginine methyltransferase I (CARM1, also known as Protein aRginine MethylTransferase 4, or PRMT4) regulates gene expression by multiple mechanisms including methylation of histones and coactivation of steroid receptor transcription. Mice lacking CARM1 are smaller than their littermates, fail to breath, and die shortly after birth, demonstrating the critical role of CARM1 in development.We performed gene expression analysis to identify genes that are responsible for hyperproliferaion in CARM1 knockout lung. RNA extracted from murine lung at E18.5 with carm1 knockouts and wild type controls was hybridised to Affymetrix mouse430.2 GeneChips to identify differentially expressed genes in the disease state.
2010-07-07 | E-GEOD-21606 | biostudies-arrayexpress
Project description:Murine lung tissue: Gremlin-1 transgenic vs. wild type
| PRJNA318808 | ENA
Project description:Transcriptional profiling of murine lung tissue comparing wild type to gremlin-1 transgenic untreated or silicon dioxide (silica)-treated for two months. Gremlin-1 transgene expression in lung type II epithelial cells under SPC promoter. Aim was to compare expression of fibrosis and inflammation associated genes.
2016-12-21 | GSE80406 | GEO
Project description:The goal of the project was global identification of CARM1 substrates. Arginine methylation landscapes were profiled and compared in wild type and CARM1 knockout cells to determine in vivo substrates of CARM1.
2017-07-03 | PXD005871 | Pride
Project description:We compared expression of genes in brains of SIRT1 brain-specific knockouts (BSKO) to those of wild-type littermate controls (WT).
2011-04-22 | GSE28790 | GEO
Project description:We hypothesize that gene expression in the cigarette smoke (CS) exposed neonatal lung and age-matched controls will be divergent. CS exposed lung will have divergence of immune response genes and structural genes. The lungs of (6) 2 week old neonatal mice exposed to 2 weeks of CS were compared to the lung of (4) 2 week old age-matched control mice. We utilized microarray analysis to examine transcriptional differences between smoke exposed neonatal lung and age-matched controls. Keywords: comparative expression profiling
2008-01-01 | GSE7310 | GEO
Project description:Growth Differentiation Factor 15 (GDF15) is a divergent member of the TGF-β superfamily, and its expression increases under various stress conditions, including inflammation, hyperoxia, and senescence. GDF15 expression is increased in neonatal murine BPD models, and GDF15 loss exacerbates oxidative stress and decreases viability in vitro in pulmonary epithelial and endothelial cells. Our overall hypothesis is that the loss of GDF15 will exacerbate hyperoxic lung injury in the neonatal lung in vivo. We exposed neonatal Gdf15-/- mice and wild-type (WT) controls on a similar background to room air or hyperoxia (95% O2) for 5 days after birth. The mice were euthanized on PND 21. Gdf15 -/- mice had higher mortality and lower body weight than WT mice after exposure to hyperoxia. Upon exposure to hyperoxia, female mice had higher alveolar simplification in the Gdf15-/- group than the female WT group. Gdf15-/- and WT mice showed no difference in the degree of the arrest in angiogenesis upon exposure to hyperoxia. Gdf15-/- mice showed lower macrophage count in the lungs compared to WT mice. Our results suggest that Gdf15 deficiency decreases the tolerance to hyperoxic lung injury with evidence of sex-specific differences.
2023-07-20 | GSE211744 | GEO
Project description:Transcriptome profile of Carm1 KO and Wildtype neonatal heart cardiomyocyte
2023-12-26 | GSE212981 | GEO
Project description:Type I interferons (IFN-I) are key innate immune mediators which control viral infection in adults. Recently, using a neonatal murine model of influenza A infection (IAV), we demonstrated that IAV-infected murine neonates lacking a functional IFN-I receptor (IFNAR-/-) have significantly improved survival and reduced lung pathology relative to wild-type (WT) neonates. However, the opposite is observed in adults, with IAV-infected IFNAR-/- adults exhibiting enhanced morbidity relative to WT adults, indicating an age-specific IFN-I toxicity in neonates. Therefore, we hypothesized that IAV-induced IFN-I signaling in primary neonatal type II alveolar epithelial cells (TIIECs), the main cell type of IAV infection and initiator of host response in the lung, contributed to age-specific viral pathogenesis. To investigate the role of IFN-I signaling in TIIECs, we performed RNA-Seq on purified TIIECs in a multifactorial design, comparing 1. IFNAR-/- and WT genotypes, 2. neonatal and adult ages, 3. IAV-infected and uninfected, 4. over a three-day time course.Analysis of purified TIIECs revealed age, not infection status, as the primary driver of transcriptional differences in TIIECs. Subsequent pathway analysis demonstrated IAV-infected IFNAR-/- neonates significantly upregulate cell proliferation, tissue repair and tight junction genes at 2-days post-infection (dpi), compared to WT neonates. Next, to determine if these growth and repair differences persisted later in infection, targeted analysis of repair gene expression and immunofluorescent quantification of pulmonary sealing tight junction molecules ZO-1 and occludin was performed at 6-dpi. Relative to WT neonates, IFNAR-/- neonates had significantly higher whole lung occludin staining and repair gene expression. Together, our data demonstrates IFN-I signaling is extremely pathogenic in the developing lung because by disrupting alveolar repair and pulmonary barrier integrity.
2025-02-22 | GSE287098 | GEO
Project description:Genome-wide transcriptome analysis of the neonatal control and Carm1 mutant hearts
2023-12-26 | GSE197196 | GEO