Mus musculus strain:C57BL/6J
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ABSTRACT:
PROVIDER: PRJDB18374 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptome analysis of epithelial cells in the small intestine of wild-type and vasopressin receptor-deficient mice
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Project description:RNA-Seq, Sufficiently atrophied soleus and EDL muscle tissues of mice
| PRJDB15791 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE8549: Transcriptome of reloaded soleus muscle of 129/SV mice GSE8550: Transcriptome of soleus muscle of Tenascin-C deficient 129/SV mice GSE8551: Transcriptome of reloaded soleus muscle of Tenascin-C deficient 129/SV mice GSE8552: Transcriptome of soleus muscle of 129/SV mice Keywords: SuperSeries Refer to individual Series
2010-06-25 | E-GEOD-10050 | biostudies-arrayexpress
Project description:Soleus muscle from Eif6 heterozygous mice and wild-type mice profiled using Agilent gene expression arrays
2018-07-07 | GSE116714 | GEO
Project description:The ability to generate defined null mutations in mice revolutionized the analysis of gene function in mammals. However, gene-deficient mice generated by using 129-derived embryonic stem (ES) cells may carry large segments of 129 DNA, even when extensively backcrossed to reference strains, such as C57BL/6J, and this may confound interpretation of experiments performed in these mice. Tissue plasminogen activator (tPA), encoded by the PLAT gene, is a fibrinolytic serine protease that is widely expressed in the brain. A large number of neurological abnormalities have been reported in tPA-deficient mice. The studies here compare genes differentially expressed in the brains of Plat-/- mice from two independent Plat-/- mouse derivations to wild-type C57BL/6J mice. One strain denoted “Old” was constructed in ES cells from a 129 mouse and backcrossed extensively to C57BL/6J, and one denoted “New” Plat-/- mouse was constructed using zinc finger nucleases directly in the C57BL/6J-Plat-/- mouse strain. We identify a significant set of genes that are differentially expressed in the brains of Old Plat-/- mice that preferentially cluster in the vicinity of Plat on chromosome 8, apparently linked to more than 20 Mbp of DNA flanking Plat being of 129 origin. No such clustering is seen in the New Plat-/- mice.
2016-12-16 | GSE76093 | GEO
Project description:In order to identify gene expression patterns that vary with diet, genetics, and their interaction, we performed expression profiling by RNA-Seq across four different tissues (liver, gonadal fat, soleus muscle, and pancreas) of TALLYHO/Jng (TH) and C57BL/6J (B6) male (M) and female (F) mice, fed either a chow or high fat (HF) diet at 5 weeks and 20 weeks of age.
2023-11-30 | GSE234011 | GEO
Project description:We performed RNA-Seq for brwon fat, epididymal white fat and soleus muscle of mice to identify brown fat-selective, white fat-selective and common fat genes. RNA-Seq for brown fat, white fat and soleus muscle of wild type C56BL6 mice.
2015-12-31 | E-GEOD-56367 | 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. 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:Myofiber size regulation is critical in health, disease, and aging. MuSK (muscle-specific kinase) is a BMP (bone morphogenetic protein) co-receptor that promotes and shapes BMP signaling that is expressed at all neuromuscular junctions and is also present extrasynaptically in the slow soleus muscle. To investigate the role of the MuSK-BMP pathway in vivo we generated mice lacking the BMP-binding MuSK Ig3 domain. These ∆Ig3-MuSK mice are viable and fertile with innervation levels comparable to wild type. In 3-month-old mice myofibers are smaller in the slow soleus, but not in the fast TA. Here we use bulk RNA-seq to perform transcriptomic analysis of slow and fast mouse muscle. RNAseq analysis revealed soleus-selective decreases in RNA metabolism and protein synthesis pathways as well as dysregulation of IGF1 pathway components. Moreover, Akt-mTOR signaling is reduced in soleus but not TA. We propose that the MuSK-BMP pathway acts extrasynaptically to maintain myofiber size in slow muscle by promoting protein synthetic pathways including the IGF1-Akt-mTOR signaling. These results reveal a novel mechanism for regulating myofiber size in slow muscle and introduce the MuSK-BMP pathway as a target for promoting muscle growth and combatting atrophy.
2024-01-10 | GSE212352 | GEO