Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA401689 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression of macrophages and microglia from naïve or MHV infected mouse brains
| PRJNA406878 | ENA
Project description:We use microarray analysis to compare the expression profiles of glioma-associated microglia/macrophages and naive control cells. Samples were generated from CD11b+ MACS-isolated cells from naïve and GL261-implanted C57BL/6 mouse brains.
2014-12-31 | E-MTAB-2660 | biostudies-arrayexpress
Project description:PURPOSE: To provide a detailed gene expression profile of the normal postnatal mouse cornea. METHODS: Serial analysis of gene expression (SAGE) was performed on postnatal day (PN)9 and adult mouse (6 week) total corneas. The expression of selected genes was analyzed by in situ hybridization. RESULTS: A total of 64,272 PN9 and 62,206 adult tags were sequenced. Mouse corneal transcriptomes are composed of at least 19,544 and 18,509 unique mRNAs, respectively. One third of the unique tags were expressed at both stages, whereas a third was identified exclusively in PN9 or adult corneas. Three hundred thirty-four PN9 and 339 adult tags were enriched more than fivefold over other published nonocular libraries. Abundant transcripts were associated with metabolic functions, redox activities, and barrier integrity. Three members of the Ly-6/uPAR family whose functions are unknown in the cornea constitute more than 1% of the total mRNA. Aquaporin 5, epithelial membrane protein and glutathione-S-transferase (GST) omega-1, and GST alpha-4 mRNAs were preferentially expressed in distinct corneal epithelial layers, providing new markers for stratification. More than 200 tags were differentially expressed, of which 25 mediate transcription. CONCLUSIONS: In addition to providing a detailed profile of expressed genes in the PN9 and mature mouse cornea, the present SAGE data demonstrate dynamic changes in gene expression after eye opening and provide new probes for exploring corneal epithelial cell stratification, development, and function and for exploring the intricate relationship between programmed and environmentally induced gene expression in the cornea. Keywords: other
2004-01-02 | GSE887 | GEO
Project description:We conducted a comprehensive analysis of the proteome of mouse bone marrow dendritic cells (BMDCs) infected with MHV-A59. We characterized the global gene changes at the protein levels following viral infection, identifying ten genes involved in various anti-MHV biological processes.
2025-06-06 | PXD061826 | Pride
Project description:Gene expression of macrophages isolated from mouse brains
| PRJNA401690 | ENA
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Murine gammaherpesvirus 68 (MHV-68) is closely related to Epstein-Barr virus (EBV) and KaposiM-bM-^@M-^Ys sarcoma-associated herpesvirus (KSHV) and provides a small animal model to study the pathogenesis of gammaherpesvirus (M-NM-3HV) infections. To completely explore the potential of the MHV-68 system for the investigation of gHV miRNAs, it would be desirable to know the number and expression patterns of all miRNAs encoded by MHV-68. By using small RNA deep sequencing, we systematically investigated the MHV-68 miRNA expression profiles in both lytically and persistently infected cells. In addition to the known nine MHV-68 miRNAs, we identified six novel MHV-68 miRNA genes and analyzed the expression levels of all MHV-68 miRNAs. Furthermore, we also characterized the cellular miRNA expression signatures in MHV-68 infected versus non-infected NIH3T3 fibroblasts and in TPA-treated versus non-treated S11 cells. We found that mmu-mir-15b and mmu-mir-16 are highly upregulated upon MHV-68 infection of NIH3T3 cells, indicating a potential role of cellular miRNAs during MHV-68 infection. Our data will aid to fully explore the functions of gHV miRNAs. A mouse fibroblast cell line infected with/without MHV-68 and a MHV-68 infected mouse B lymphoma cell line treated with/without TPA (4 samples in total) were examined.
2010-07-15 | E-GEOD-22938 | biostudies-arrayexpress
Project description:Engrams are considered to be substrates for memory storage, and the functional dysregulation of the engrams leads to cognition impairment.However, the cellular basis for these maladaptive changes lead to the forgetting of memories remains unclear. Here we found that the expression of autophagy protein 7 (Atg7) mRNA was dramatically upregulated in aged DG engrams, and led to the forgetting of contextual fear memory and the activation of surrounding microglia.To determine mechanism by which autophagy in DG engrams activates the surrounding microglia, mice were co-injected AAV-RAM-Cre either with AAV-Dio-Atg7-Flag or AAV-Dio- EYFP in dorsal dentate gyrus to overexpress ATG7 in the DG memory engrams. Microglia were separated using magnetic-activated cell sorting and subjected to RNA-Seq in dorsal hippocampus .Bioinformatics analysis shown overexpression of Atg7 in dorsal DG memory engrams caused an increase in the expression of Tlr2 in the surrounding microglia.Depletion of Toll-like receptor 2/4 (TLR2/4) in DG microglia prohibited excessive microglial activation and synapse elimination induced by the overexpression of ATG7 in DG engrams, and thus prevented forgetting. Furthermore, the expression of Rac1, a Rho-GTPases which regulates active forgetting in both fly and mice, was upregulated in aged engrams. Optogentic activation of Rac1 in DG engrams promoted the autophagy of the engrams, the activation of microglia, and the forgetting of fear memory. Invention of the Atg7 expression and microglia activation attenuated forgetting induced by activation of Rac1 in DG engrams. Together, our findings revealed autophagy-dependent synapse elimination of DG engrams by microglia as a novel forgetting mechanism.
2021-08-24 | GSE169019 | GEO
Project description:Gene expression profiles of Ecrg4-treated mouse microglia
| PRJNA344559 | ENA