Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

C57BL/6 mice: Control vs. skeletal muscle-specific FoxO1 deletion (mFoxO1KO)

ABSTRACT: Transcriptional profiling of lower-limb skeletal muscle (SKM) comparing control mice and mFoxO1KO mice with skeletal muscle-specific FoxO1 deficiency. The goal was to determine the effect of skeletal muscle-specific FoxO1 deficiency on metabolic-associated gene expression in skeletal muscle.

ORGANISM(S): Mus musculus

PROVIDER: GSE226462 | GEO | 2026/02/28

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Microarray analysis of transgenic mice specifically overexpressing FOXO1 in skeletal muscle (FOXO1 Tg mice)

Project description:FOXO1, a member of the FOXO forkhead type transcription factors, is markedly up-regulated in skeletal muscle during atrophy. Previously, we created transgenic mice specifically overexpressing FOXO1 in skeletal muscle (FOXO1 Tg mice). These mice weighed less than the wildtype control mice, had a reduced skeletal muscle mass. In this study, to better understand changes in skeletal muscle during atrophy, we performed a microarray analysis of skeletal muscle in wild-type control and FOXO1 Tg mice. The microarray data shows that in the skeletal muscles of FOXO1 Tg mice, gene expression of PGC-1β, a transcriptional regulator whose increased expression activates energy-expenditure-related genes in skeletal muscles, is decreased.

2020-07-07 | GSE146919 | GEO

C57BL/6 mice: Control vs. skeletal muscle-specific FoxO1 deletion (mFoxO1KO)

Project description:C57BL/6 mice: Control vs. skeletal muscle-specific FoxO1 deletion (mFoxO1KO)

| PRJNA940388 | ENA

Regulation of Glucose Uptake and Inflammation by FOXO1 and FOXO3 in Skeletal Muscle

Project description:Forkhead box class O (FoxO) transcription factors regulate whole body energy metabolism, skeletal muscle mass and substrate switching. To elucidate the role of FOXO in skeletal muscle, dominant negative (dn) constructs for FOXO1 (FOXO1dn) or FOXO3 (FOXO3dn) were transfected by electroporation into mouse tibialis anterior muscle and glucose uptake, signal transduction, and glucose stimulated gene expression profiles were assessed. Results were compared against contralateral control transfected muscle. Transcriptomic analysis revealed major pathways affected by FOXO1dn or FOXO3dn revolve around metabolism and inflammation.

2018-12-10 | GSE105778 | GEO

Microarray analysis of transgenic mice specifically overexpressing FOXO1 in skeletal muscle (FOXO1 Tg mice)

Project description:Microarray analysis of transgenic mice specifically overexpressing FOXO1 in skeletal muscle (FOXO1 Tg mice)

| PRJNA612433 | ENA

Pantothenate kinase 4 controls skeletal muscle substrate metabolism

Project description:Metabolic flexibility in skeletal muscle is essential for maintaining healthy glucose and lipid metabolism, and its dysfunction is closely linked to metabolic diseases. Exercise enhances metabolic flexibility, making it an important tool for discovering mechanisms that promote efficient energy metabolism. We herein discover pantothenate kinase 4 (PanK4) as a conserved exercise target with high abundance in muscle. Germline deletion of Pank4 reduces circulating IGF-1 and stunts growth in mice. Muscle-specific deletion of Pank4 leads to a reduction in carnitzed and in impaired fatty acid oxidation in oxidative muscle which is related to higher acetyl-CoA and malonyl levels. Acetyl-CoA levels were persistently elevated in SkM lacking PanK4, independent of prandial state. In addition to perturbations of fatty acid oxidation, high SkM acetyl-CoA levels were associated with whole-body glucose intolerance, impaired insulin-stimulated glucose uptake into glycolytic SkM and impaired SkM glucose uptake during exercise. Conversely, we show that an increase in PanK4 lowers acetyl-CoA and increases glucose uptake in glycolytic SkM. Our findings identify PanK4 as a conserved exercise target that regulates SkM acetyl-CoA levels and plays a key role in lipid and glucose metabolism.

2024-10-25 | PXD057017 | Pride

Loss of AnkB upregulates stress-related pathways in skeletal muscle

Project description:Human mutations in the ANK2 gene, which encodes ankyrin B (AnkB), lead to age- and diet-induced metabolic syndrome in mice. To investigate the contribution of skeletal muscle (SKM) AnkB to systemic energy balance and metabolic homeostasis, we developed skeletal muscle (SKM)-specific AnkB knockout (KO) (Ank2f/f; HSA-Cre+) mice. Physiological,cellular, biochemical and transcriptional characterization of these mice uncovered a muscle-autonomous role of AnkB in maintaning mitochondria health and muscle energetic homeostasis via the regulation of mitochondrial dynamics and sarcoplasmic reticulum (SR) organization.

2025-09-03 | GSE286564 | GEO

Cardiac and skeletal muscle gene expression profiles in dysferlin deficient mice

Project description:Dysferlin is expressed in skeletal and cardiac muscle. However, dysferlin deficiency, namely limb girdle muscular dystrophy 2B (LGMD2B) and Myoshi myopathy, results in skeletal muscle weakness and spares the heart. This dichotomy could be caused by differential regulation of protective mechanisms. Therefore, we compared intraindividual mRNA expression profiles between cardiac and skeletal muscle in dysferlin-deficient SJL/J mice and normal C57BL/6 mice. Keywords: parallel sample

2005-07-10 | GSE2507 | GEO

Gene expression analysis in skeletal muscle and heart of 11 days-old TK2 knockout mice

Project description:TK2 deficiency causes severe mtDNA depeltion in several tissues, including skeletal muscle and heart. TK2 knockout mice grow slower and their skeletal muscles appeared significantly underdeveloped, whereas heart was close to normal size. We used microarrays in order to compare the transcriptomes in skeletal muscle and heart tissue of 11 days-old TK2 knockout pups with the sames tissues of wild-type pups at the same age. We collected skeletal muscle from the hind limb and hearts of three 11 days-old TK2 knockout and three wild-type pups and extracted total RNA. These RNA samples were used for hybridization in Affymetrix arrays.

2012-07-30 | E-GEOD-38449 | biostudies-arrayexpress

PAX3-FOXO1 suppresses cellular senescence through RASSF4-mediated restraint of the mammalian Hippo/MST1 pathway

Project description:Alveolar rhabdomyosarcoma (aRMS) is an aggressive sarcoma of skeletal muscle characterized by expression of the PAX3-FOXO1 fusion gene. Despite its discovery over almost 20 years ago, PAX3-FOXO1 remains an enigmatic tumor driver. Previously, we reported that PAX3-FOXO1 supports aRMS initiation by enabling bypass of cellular senescence. Here, we show that bypass occurs in part by PAX3-FOXO1-mediated upregulation of RASSF4, a Ras-association domain family (RASSF) member, which then suppresses the evolutionarily conserved mammalian Hippo/Mst1 pathway. RASSF4 loss-of-function activates Hippo/Mst1 and inhibits downstream YAP, causing aRMS cell cycle arrest and senescence. This is the first evidence for an oncogenic role for RASSF4, and a novel mechanism for Hippo signaling suppression in human cancer. Human skeletal muscle myoblasts (HSMMs) were retrovirally transduced with either an empty vector (Vp, pK1) or PAX3-FOXO1 (PFp, pK1-PAX3-FOXO1) and selected on puromycin. Presenescent (presen) cells were harvested before the senescence checkpoint. Since cells expressing PAX3-FOXO1 can bypass the senescence checkpoint, postsenescent (postsen) cells expressing PAX3-FOXO1 were also harvested. the gene expression affected by the introduction of PAX3-FOXO1

2014-05-15 | E-GEOD-40543 | biostudies-arrayexpress

Exercise alleviates cognitive dysfunction in Alzheimer’s disease mice via skeletal muscle-derived extracellular vesicles which enhance plaque clearance by microglia [RNA-Seq]

Project description:Exercise confers cognitive benefits in Alzheimer’s disease (AD), yet the underlying mechanisms remain incompletely understood. The skeletal muscle functions as an endocrine organ that secretes myokines which affect the homeostasis of extra-muscular organs, including the brain. Here, we found that swimming exercises promoted the secretion of skeletal muscle-derived extracellular vesicles (SKM-EVs), which subsequently pinocytosis by microglia. Gain- and loss-of-function experiments showed that exercised SKM-EVs activated the polarization of disease-associated microglia (DAM) and enhanced the clearance of amyloid-beta (Aβ) plaques. Furthermore, miR-378a-3p was identified as the key miRNA in SKM-EVs and promoted lipid metabolism in DAM by targeting p110α. Importantly, the therapeutic administration of EVs derived from mir-378a overexpressing myotubes alleviated cognitive impairment in AD mice. Together, our findings demonstrate that exercised SKM-EVs could serve as a novel myokine mediating communication from skeletal muscle to the brain and develop alternative therapeutic strategies for exercise in AD treatment.

2025-12-18 | GSE313455 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data