Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126685 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride
Project description:Microarray skeletal muscle miR-499 overexpressing mice
| PRJNA294413 | ENA
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2018-04-24 | PXD007288 | Pride
Project description:microRNAs are small non-coding RNAs that can affect gene expression. We used microarrays to analyze gene expression in miR-499 transgenic mouse hearts. Cardiac ventricles were collected at postnatal day 17 from wild type and miR-499 transgenics.
2011-05-31 | E-GEOD-21104 | biostudies-arrayexpress
Project description:This experiment was conducted to identify target genes of the microRNA-499 in skeletal muscle of transgenic mice that overexpressed miR-499. The following abstract from the submitted manuscript describes the major findings of this work. Coupling of mitochondrial function and skeletal muscle fiber type by a miR-499/Fnip1/AMPK circuit. Jing Liu, Xijun Liang, Danxia Zhou, Ling Lai, Tingting Fu, Yan Kong, Qian Zhou, Rick B. Vega, Min-Sheng Zhu, Daniel P. Kelly, Xiang Gao, and Zhenji Gan. Upon adaption of skeletal muscle to physiological and pathophysiological stimuli, muscle fiber type and mitochondrial function are coordinately regulated. Recent studies have identified pathways involved in control of contractile proteins of oxidative type fibers. However, the mechanism for coupling of mitochondrial function to muscle contractile machinery during fiber type transition remains unknown. Here, we show that the expression of the genes encoding type I myosins, Myh7/Myh7b and their intronic miR-208b/miR-499 parallels mitochondrial function during fiber type transitions. Using in vivo approaches in mice, we found that miR-499 drives a PGC-1a-dependent mitochondrial oxidative metabolism program to match shifts in slow-twitch muscle fiber composition. Mechanistically, miR-499 directly targets Fnip1, a known AMP-activated protein kinase (AMPK)-interacting protein that negatively regulates AMPK, a known activator of PGC-1a. Inhibition of Fnip1 reactivated AMPK/PGC-1a signaling and mitochondrial function in myocytes. Restoration of the expression of miR-499 in the mdx mouse model of Duchenne muscular dystrophy (DMD) reduced the severity of DMD. Thus, we have identified a miR-499/Fnip1/AMPK circuit that can serve as a mechanism to couple muscle fiber type and mitochondrial function. Keywords: muscle, contractile fiber type, mitochondrial function, microRNA, gene regulation RNA from three wild-type (non-transgenic (NTG)) and three miR-499 overexpressing (MCK-miR-499) mice was analyzed. three replicates of each are provided.
2016-09-03 | E-GEOD-72581 | biostudies-arrayexpress
Project description:This experiment was conducted to identify target microRNAs of the peroxisome proliferator-activated receptor (PPAR) in skeletal muscle of transgenic mice that overexpressed PPARalpha or PPARbeta. We have recently demonstrated that skeletal muscle-specific PPARb transgenic (MCK-PPARb) mice exhibit increased exercise endurance, whereas MCK-PPARa mice have reduced exercise performance. Accordingly, we sought to determine whether PPARb and PPARa drive distinct programs involved in muscle fiber type determination. Myosin heavy chain (MHC) immunohistochemical staining of soleus muscle revealed a marked increase in type 1 fibers in the MCK-PPARb muscle compared to non-transgenic (NTG) littermates but a profound reduction in MCK-PPARa muscle. miRNA profiling revealed that levels of miR-208b and miR-499 were increased in MCK-PPARb muscle but reduced in MCK-PPARa muscle. miR-208b and miR-499, which are embedded in the Myh7 and Myh7b genes, respectively, have been shown previously to regulate slow-twitch muscle genes. Lastly, combined inhibition of miR-208b and miR-499 abolished the enhancing effects of PPARb on MHC1 expression in skeletal myotubes, while forced expression of miR-499 in MCK-PPARa muscle completely reversed the type 1 fiber program and exercise capacity. Taken together, these findings demonstrate that miR-208b and miR-499 are necessary to mediate the effects of PPARb and PPARa on muscle fiber type determination.
2013-05-09 | GSE36498 | GEO
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature
Project description:This experiment was conducted to identify target microRNAs of the peroxisome proliferator-activated receptor (PPAR) in skeletal muscle of transgenic mice that overexpressed PPARalpha or PPARbeta. We have recently demonstrated that skeletal muscle-specific PPARb transgenic (MCK-PPARb) mice exhibit increased exercise endurance, whereas MCK-PPARa mice have reduced exercise performance. Accordingly, we sought to determine whether PPARb and PPARa drive distinct programs involved in muscle fiber type determination. Myosin heavy chain (MHC) immunohistochemical staining of soleus muscle revealed a marked increase in type 1 fibers in the MCK-PPARb muscle compared to non-transgenic (NTG) littermates but a profound reduction in MCK-PPARa muscle. miRNA profiling revealed that levels of miR-208b and miR-499 were increased in MCK-PPARb muscle but reduced in MCK-PPARa muscle. miR-208b and miR-499, which are embedded in the Myh7 and Myh7b genes, respectively, have been shown previously to regulate slow-twitch muscle genes. Lastly, combined inhibition of miR-208b and miR-499 abolished the enhancing effects of PPARb on MHC1 expression in skeletal myotubes, while forced expression of miR-499 in MCK-PPARa muscle completely reversed the type 1 fiber program and exercise capacity. Taken together, these findings demonstrate that miR-208b and miR-499 are necessary to mediate the effects of PPARb and PPARa on muscle fiber type determination. Comparison of microRNA expression from soleus muscles isolated from wild-type (non-transgenic (NTG)) and PPARalpha-overexpressing (MCK-PPARa) mice, and comparison of microRNA expression from soleus muscles isolated from wild-type (NTG) and PPARbeta-overexpressing (MCK-PPARb) mice. Three replicates of each are analyzed.
2013-05-09 | E-GEOD-36498 | biostudies-arrayexpress
Project description:To explore the role of miR-22 in the heart, we generated miR-22 null and transgenic mice. Absence of miR-22 results in partial embryonic lethality arising from cardiac malformations. miR-22-null mice that survived until adulthood showed normal cardiac structure and function at baseline but were sensitized to cardiac dysfunction and dilation following pressure overload stimulation. Absence of miR-22 prevented the induction of beta-myosin heavy chain (Myh7) and miR-208b expression following pathologic stress. miR-22 null animals were also compromised in cardiac expression of Myh7b and miR-499. We found that miR-22 directly regulates two transcriptional antagonists, purine rich element binding protein B (PURB), a repressor, and serum response factor (SRF), an activator, in the heart. Through these gain- and loss-of-function experiments in mice, we suggest that a primary function of miR-22 is to fine tune the relative expression and activity of these two transcriptional antagonists to influence contractile gene expression, function, growth and adaptation of the heart to stress.
2012-09-11 | E-MTAB-500 | biostudies-arrayexpress
Project description:Expression analysis of eu-miR-155 transgenic mice B-cells.
| PRJNA143781 | ENA