E-GEOD-16360
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-16360 | ExpressionAtlas | 2015-09-03
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE16360: Gene expression profiling of muscles from transgenic humanSODG93A mice at presymptomatic stage GSE16361: Gene expression profiling of muscles from transgenic humanSODG93A mice at symptomatic stage Refer to individual Series
2009-06-02 | E-GEOD-16362 | biostudies-arrayexpress
Project description:Gene expression profiling of muscles from transgenic humanSODG93A mice at presymptomatic stage
| PRJNA122849 | ENA
Project description:Gene expression profiling of muscles from transgenic humanSODG93A mice at symptomatic stage
| PRJNA122851 | ENA
Project description:Gene expression profiling of muscles from transgenic humanSODG93A mice at symptomatic stage
2015-09-03 | E-GEOD-16361 | ExpressionAtlas
Project description:PGC1b transgenic mice were generated to selectively over-express PGC1b in skeletal muscles using human skeletal alpha-actin gene promoter. The gene expression profiles were collected from Tibialis anterior (TA) muscles of wild type (WT) and PGC1b transgenic (TG) mice.
2014-06-21 | GSE58699 | GEO
Project description:PGC1b transgenic mice were generated to selectively over-express PGC1b in skeletal muscles using human skeletal alpha-actin gene promoter. The gene expression profiles were collected from Tibialis anterior (TA) muscles of wild type (WT) and PGC1b transgenic (TG) mice. Tibialis anterior muscles from three month old WT and PGC1b transgenic male mice.
2014-06-21 | E-GEOD-58699 | biostudies-arrayexpress
Project description:We analyzed the gene expression changes that result from mitochondria overloaded by unfolded proteins in skeletal muscles. Mitochondrial-retained mutant ornithine transcarbamylase (ΔOTC) is a known protein degraded by LONP1 and an established model for studying mitochondrial proteostasis imbalance. We generated transgenic mice overexpressing ΔOTC specifically in skeletal muscle using the muscle creatine kinase promoter (MCK-ΔOTC). Transcriptome analysis was performed by whole-genome gene expression profiling experiments in muscles from the MCK-ΔOTC mice and NTG littermate controls. The comparative mRNA profiling strategy revealed extensive genomic reprogramming in MCK-ΔOTC muscles, with 1051 genes up- and 519 genes down-regulated (1.5-fold change and p<0.05), respectively. GO analysis of the regulated genes in MCK-ΔOTC muscles revealed significant enrichment in unfolded protein response as well as RNA processing process. These data suggest that mitochondria overloaded by ΔOTC unfolded proteins induce extensive genomic reprogramming in skeletal muscle
2022-07-28 | GSE192991 | GEO
Project description:Transgenic overexpression of Galgt2 in the skeletal muscles of mdx mice inhibits the development of disease pathology associated with muscular dystrophy. This is the case both in transgenic mice, where Galgt2 overexpression occurs from embryonic timepoints onward and in mdx mice where Galgt2 is overexpressed in the early postnatal period using Adeno-associated virus (AAV). Here, we use gene expression profiling to compare transcriptional changes resulting from embryonic and postnatal Galgt2 overexpression in mdx skeletal muscle. A surprising number of changes were in genes known to ameliorate muscular dystrophy when overexpressed (agrin, integrin alpha 7, ADAM12, Bcl2) or to cause muscular dystrophy when mutated (collagen VI (alpha1,alpha2), plectin 1, dystroglycan, selenoprotein N1, integrin alpha7, biglycan, dysferlin). Several genes involved in calcium homeostasis were also changed. In Galgt2 transgenic mice, where embryonic overexpression of Galgt2 in skeletal muscles alters neuromuscular development and muscle growth, the number of gene expression changes was vastly greater, however, 14% of genes altered in postnatal AAV-Galgt2 infected mdx muscles were also changed with embryonic overexpression. These experiments suggest that postnatal overexpression of Galgt2 inhibits muscular dystrophy in mdx mice via induction of a group of genes that, in aggregate, can govern membrane stability, membrane repair, calcium homeostasis, and apoptosis. Transgenic overexpression of Galgt2 in the skeletal muscles of mdx mice inhibits the development of disease pathology associated with muscular dystrophy. This is the case both in transgenic mice, where Galgt2 overexpression occurs from embryonic timepoints onward and in mdx mice where Galgt2 is overexpressed in the early postnatal period using Adeno-associated virus (AAV). Here, we use gene expression profiling to compare transcriptional changes resulting from embryonic and postnatal Galgt2 overexpression in mdx skeletal muscle. A surprising number of changes were in genes known to ameliorate muscular dystrophy when overexpressed (agrin, integrin alpha7, ADAM12, Bcl2) or to cause muscular dystrophy when mutated (collagen VI (alpha1,alpha2), plectin 1, dystroglycan, selenoprotein N1, integrin alpha7, biglycan, dysferlin). Several genes involved in calcium homeostasis were also changed. In Galgt2 transgenic mice, where embryonic overexpression of Galgt2 in skeletal muscles alters neuromuscular development and muscle growth, the number of gene expression changes was vastly greater, however, 14% of genes altered in postnatal AAV-Galgt2 infected mdx muscles were also changed with embryonic overexpression. These experiments suggest that postnatal overexpression of Galgt2 inhibits muscular dystrophy in mdx mice via induction of a group of genes that, in aggregate, can govern membrane stability, membrane repair, calcium homeostasis, and apoptosis. Experiment Overall Design: Microarrays were done in three groups at a time. 1) Transgenic Overexpression of Galgt2 - comprised to Wild Type (WT), Galgt2 Transgenic (CT), Dystrophin-Deficient (mdx), and Galgt2 Transgenic and Dystrophin-Deficient (CTmdx) each in duplicate 2) AAV-Mediated Galgt2 Gene Delivery in to the mdx gastrocnemius muscle in the postnatal period - comprised of AAVGalgt2 and PBS each in duplicate, and 3) Myoblasts and myotubes - comptised of one sample each of C1C12 myoblasts and myotubes, C2C12 myoblasts and myotubes stably transfected with Galgt2
2009-03-07 | E-GEOD-7863 | biostudies-arrayexpress
Project description:Transgenic overexpression of Galgt2 in the skeletal muscles of mdx mice inhibits the development of disease pathology associated with muscular dystrophy. This is the case both in transgenic mice, where Galgt2 overexpression occurs from embryonic timepoints onward and in mdx mice where Galgt2 is overexpressed in the early postnatal period using Adeno-associated virus (AAV). Here, we use gene expression profiling to compare transcriptional changes resulting from embryonic and postnatal Galgt2 overexpression in mdx skeletal muscle. A surprising number of changes were in genes known to ameliorate muscular dystrophy when overexpressed (agrin, integrin alpha 7, ADAM12, Bcl2) or to cause muscular dystrophy when mutated (collagen VI (alpha1,alpha2), plectin 1, dystroglycan, selenoprotein N1, integrin alpha7, biglycan, dysferlin). Several genes involved in calcium homeostasis were also changed. In Galgt2 transgenic mice, where embryonic overexpression of Galgt2 in skeletal muscles alters neuromuscular development and muscle growth, the number of gene expression changes was vastly greater, however, 14% of genes altered in postnatal AAV-Galgt2 infected mdx muscles were also changed with embryonic overexpression. These experiments suggest that postnatal overexpression of Galgt2 inhibits muscular dystrophy in mdx mice via induction of a group of genes that, in aggregate, can govern membrane stability, membrane repair, calcium homeostasis, and apoptosis. Keywords: disease state analysis, gene therapy, comparative gene expression, muscular dystrophy, glycosylation, collagens, integrins, dysferlin, dystroglycan
2009-03-01 | GSE7863 | GEO
Project description:Cancer is considered as a disease of a specific organ, but its effects are felt throughout the body. The systemic effects of cancer can lead to weakness in muscles and heart, which hastens cancer-associated death. miR-486 is a myogenic microRNA and its reduced expression in skeletal muscle is observed in muscular dystrophy. Muscle-specific transgenic expression of miR-486 using muscle creatine kinase promoter (MCK-miR-486) partially rescues skeletal muscle defects in muscular dystrophy animal models. We had previously demonstrated reduced circulating and skeletal muscle levels of miR-486 in several cancer types and lower miR-486 levels correlated with skeletal muscle defects and functional limitations in mammary tumor models. Therefore, skeletal muscle defects induced by cancer could resemble defects observed in various dystrophies, which could be reversed through skeletal muscle expression of miR-486. We performed functional limitations studies and biochemical analysis of skeletal muscles of MMTV-Neu transgenic mice that mimic HER2+ breast cancer and MMTV-PyMT transgenic mice that mimic luminal subtype B breast cancer and these mice crossed to MCK-miR-486 transgenic mice. miR-486 significantly prevented tumor-induced reduction in muscle contraction force, grip strength, and rotarod performance in MMTV-Neu, but not in MMTV-PyMT mice. In MMTV-Neu model, miR-486 reversed several of the cancer-induced changes in skeletal muscle including loss of p53, phospho-AKT, and phospho-laminin alpha 2 (LAMA2) and gain of phosphorylation of the pre-mRNA processing factor hnRNPA0 and the splicing factor SRSF10. LAMA2 is a part of the dystrophin-associated glycoprotein complex, and its loss-of-function mutation is associated with congenital muscular dystrophy. Thus, similar to muscular dystrophy, miR-486 has the potential to reverse skeletal muscle defects and cancer burden in select cancer types.
2022-05-19 | PXD028554 | Pride