Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA96327 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Keywords: knockout mice, nicotinic acetylcholine receptor
2006-09-22 | GSE5320 | GEO
Project description:Studies using mice with beta4 nicotinic acetylcholine receptor (nAChR) subunit deficiency (beta4-/- mice) helped reveal the roles of this subunit in bradycardiac response to vagal stimulation, nicotine-induced seizure activity and anxiety. In order to identify genes that might be related to beta4-containing nAChRs activity, we compared the mRNA expression profiles of brains from beta4-/- and wild-type mice using Affymetrix U74Avr2 microarray. Experiment Overall Design: The experimental groups included six wild-type mice and five beta4-/- mice. All mice were 6-9 weeks old. Total RNA was extracted from whole brain tissue of the mice.
2007-11-27 | E-GEOD-5320 | biostudies-arrayexpress
Project description:This manuscript is a companion paper to Ulleryd M.U. et al (1). Data shown here include RNA sequencing data from whole aorta of ApoE-/- mice treated with the alpha 7 nicotinic acetylcholine receptor (α7nAChR) agonist AZ6983 for 8 weeks using subcutaneously implanted osmotic minipumps. 1. Ulleryd MA, Mjornstedt F, Panagaki D, Yang LJ, Engevall K, Gutierrez S, et al. Stimulation of alpha 7 nicotinic acetylcholine receptor (α7nAChR) inhibits atherosclerosis via immunomodulatory effects on myeloid cells Re-submitted. 2019.
2019-10-29 | GSE131162 | GEO
Project description:Aging is accompanied by expression changes in multiple genes and the brain is one of the tissues most vulnerable to aging. Since the alpha7 nicotinic acetylcholine receptor (nAChR) subunit has been associated with neurodevelopmental disorders and cognitive decline during aging, we hypothesized that its absence might affect gene expression profiles in aged brains. To study whether transcriptional changes occur due to aging, alpha7 deficiency or both, we analyzed whole brain transcriptomes of young (8 week) and aged (2 year) alpha7 deficient and wild-type control mice, using Mouse Genome 430 2.0 microarray. Highly significant expression changes were detected in 47 and 1543 genes (after Bonferroni and FDR correction) in the brains of aged mice compared to young mice, regardless of their genotype. These included genes involved in immune system function and ribosome structure, as well as genes that were previously demonstrated as differentially expressed in aging human brains. Genotype-dependent changes were detected in only 3 genes, Chrna7 which encodes the alpha7 nAChR subunit, and two closely linked genes, likely due to a mouse background effect. Expression changes dependent on age-genotype interaction were detected in 207 genes (with a low significance threshold). Age-dependent differential expression levels were approved in all nine genes that were chosen for validation by real-time RT-PCR. Our results suggest that the robust effect of aging on brain transcription clearly overcomes the almost negligible effect of alpha7 nAChR subunit deletion, and that germline deficiency of this subunit has a minor effect on brain expression profile in aged mice. Total of 20 samples. 10 from young adult mice (8 weeks) and 10 from aged mice (2 years). In each age group, 5 were wild-type control mice and 5 alpha7 nAChR subunit defecient mice
2011-01-01 | E-GEOD-20411 | biostudies-arrayexpress
Project description:Aging is accompanied by expression changes in multiple genes and the brain is one of the tissues most vulnerable to aging. Since the alpha7 nicotinic acetylcholine receptor (nAChR) subunit has been associated with neurodevelopmental disorders and cognitive decline during aging, we hypothesized that its absence might affect gene expression profiles in aged brains. To study whether transcriptional changes occur due to aging, alpha7 deficiency or both, we analyzed whole brain transcriptomes of young (8 week) and aged (2 year) alpha7 deficient and wild-type control mice, using Mouse Genome 430 2.0 microarray. Highly significant expression changes were detected in 47 and 1543 genes (after Bonferroni and FDR correction) in the brains of aged mice compared to young mice, regardless of their genotype. These included genes involved in immune system function and ribosome structure, as well as genes that were previously demonstrated as differentially expressed in aging human brains. Genotype-dependent changes were detected in only 3 genes, Chrna7 which encodes the alpha7 nAChR subunit, and two closely linked genes, likely due to a mouse background effect. Expression changes dependent on age-genotype interaction were detected in 207 genes (with a low significance threshold). Age-dependent differential expression levels were approved in all nine genes that were chosen for validation by real-time RT-PCR. Our results suggest that the robust effect of aging on brain transcription clearly overcomes the almost negligible effect of alpha7 nAChR subunit deletion, and that germline deficiency of this subunit has a minor effect on brain expression profile in aged mice.
2011-01-01 | GSE20411 | GEO
Project description:Bulk RNAseq from whole Drosophila melanogaster guts expressing either mCherry-RNAi (control) or RNAi against nicotinic acetylcholine receptor subunits β1 and β3 (nAchRβ1 and nAchRβ3) under control of a enterocyte-specific driver to assess their role in barrier function.
2023-08-23 | GSE236069 | GEO
Project description:Mice lacking the beta 2 subunit (Chrnb2) of the neuronal nicotinic acetylcholine receptor display altered retinal waves and disorganized projections of the retinal ganglion cells to the lateral geniculate nucleus (LGN). mRNA populations from retinas and LGN from Chrnb2-/-and wild type (C57BL/6J) mice were compared at 4 days postnatal, when RGC segregation to the LGN begins in WT mice. Retinal mRNAs were also compared at adulthood. Using microarray hybridization, we identified transcripts which are differentially expressed between Chrnb2-/- and wild type animals in these two tissues at these two ages.
2011-01-01 | GSE22824 | GEO
Project description:Mice lacking the beta 2 subunit (Chrnb2) of the neuronal nicotinic acetylcholine receptor display altered retinal waves and disorganized projections of the retinal ganglion cells to the lateral geniculate nucleus (LGN). mRNA populations from retinas and LGN from Chrnb2-/-and wild type (C57BL/6J) mice were compared at 4 days postnatal, when RGC segregation to the LGN begins in WT mice. Retinal mRNAs were also compared at adulthood. Using microarray hybridization, we identified transcripts which are differentially expressed between Chrnb2-/- and wild type animals in these two tissues at these two ages. mRNA was isolated from retina and LGN of three male littermates each of WT and Chrnb2-/- mice at P4. mRNA from retinas of two adult male littermates of each type was also examined.
2011-01-01 | E-GEOD-22824 | biostudies-arrayexpress
Project description:Bulk RNA expression profiles were captured from hearts of alpha7 nicotinic acetylcholine receptor (Chrna7) knockout (KO) and wild type (WT) mice that underwent myocardial infarction (MI) or sham (SH) surgery at postnatal day 1 and full ventricle collection at 7 days post-surgery
2021-09-28 | GSE184792 | GEO
Project description:We sequenced mRNA from 7 microglia extracted from sheep fetuses exposed to LPS, agonist and antagonist of α7 nicotinic acetylcholine receptor to determine signaling pathway through modeling of α7 during inflammation.
2017-08-11 | GSE101857 | GEO