Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KLF15- and glucocorticoid-dependent transcriptional responses in mouse muscle.

ABSTRACT: Excessive or sustained glucocorticoid (GC) exposure causes muscle wasting. Paradoxically, moderate or transient GC exposure elicits ergogenic effects, evidenced by their widespread use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle wasting disease. While mechanisms underlying GC-mediated muscle wasting are well defined, the molecular basis for the latter remains unknown. In this arm of our studies, Wild-type (WT) and Klf15-/- (KO) mice were given the potent GC receptor agonist dexamethasone (dex) and quadriceps tissue was subjected to transcript expression profiling by cDNA microarrays.

ORGANISM(S): Mus musculus

PROVIDER: GSE74624 | GEO | 2015/12/01

SECONDARY ACCESSION(S): PRJNA301032

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptional effects of forced KLF15 over-expression in mouse muscle.

Project description:Excessive or sustained glucocorticoid (GC) exposure causes muscle wasting. Paradoxically, moderate or transient GC exposure elicits ergogenic effects, evidenced by their widespread use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle wasting disease. While mechanisms underlying GC-mediated muscle wasting are well defined, the molecular basis for the latter remains unknown. In this arm of our studies, we compare expression profiles in quadriceps tissue from KLF15 transgenic (MTg) and non-Tg mice.

2015-12-01 | GSE74623 | GEO

Transcription profiling of mouse livers and quadriceps muscles of Kruppel-like factor 15 (KLF15) null mutants after an overnight fast to provide insight into the role of KLF15 in gluconeogenesis

Project description:We used microarray analysis to identify differences in gene expression levels, in liver and in quadriceps skeletal muscle, between 18h (overnight) fasted WT control and Kruppel-like factor 15 (KLF15)-null mice. Experiment Overall Design: Liver and skeletal muscle (quadriceps) tissues were isolated from 4-5 month old, 18h-fasted WT and KLF15-null female mice for RNA extraction and hybridization on Affymetrix microarrays.

2007-11-07 | E-GEOD-7137 | biostudies-arrayexpress

Transcriptional effects of KLF15 deletion in quadriceps muscle

Project description:We report bulk RNA-sequencing of quadriceps muscle harvested from MyoCre and skeletal muscle specific KLF15 (K15-SKO) mice

2021-02-17 | GSE160877 | GEO

Transcriptional effects of KLF15 deletion in quadriceps muscle

Project description:Transcriptional effects of KLF15 deletion in quadriceps muscle

| PRJNA674758 | ENA

Expression data from 18h-fasted WT versus KLF15-null mice: liver and quadriceps skeletal muscle

2007-04-02 | GSE7137 | GEO

KLF15

Project description:KLF15

| PRJNA301030 | ENA

Transcriptional effects of KLF15 deletion in soleus muscle

Project description:We report bulk RNA-sequencing of soleus muscle harvested from MyoCre and skeletal muscle specific KLF15 (K15-SKO) mice

2021-02-17 | GSE160848 | GEO

KLF15 and PPARδ cooperativity in the orchestration of lipid metabolism

Project description:We characterize the KLF15 cistrome in vivo in skeletal muscle and find that the majority of KLF15 binding is localized to distal intergenic regions and associated with genes related to circadian rhythmicity and lipid metabolism. We identify critical interdependence between KLF15 and the nuclear receptor PPARδ in the regulation of lipid metabolic gene programs. We further demonstrate that KLF15 and PPARδ co-localize genome-wide, interact, and are dependent on one another to exert their transcriptional effects on target genes.

2022-03-31 | GSE199547 | GEO

Genome-wide transcriptional targets of KLF15 in human airway smooth muscle

Project description:We previously demonstrated that the transcription factor, KLF15, is a glucocorticoid-regulated gene that represses primary human airway smooth muscle (ASM) proliferation. Here, we show that KLF15 also represses ASM hypertrophy. To uncover the mechanistic basis for these effects, we integrated transcriptome data from KLF15 over-expression with genome-wide analysis of RNA Polymerase II (RNAPII) and glucocorticoid receptor (GR) occupancy (i.e. ChIP-seq). This led us to identify PLCD1 as both a KLF15-regulated gene and a repressor of ASM hypertrophy.

2017-05-01 | GSE95397 | GEO

KLF15 Cistromes Reveal a Hepatocyte Pathway Governing Plasma Corticosteroid Transport and Systemic Inflammation

Project description:Circulating corticosteroids orchestrate stress adaptation, including inhibition of inflammation. While pathways governing corticosteroid biosynthesis and intracellular signaling are understood, less is known about mechanisms controlling plasma corticosteroid transport. Here, we show hepatocyte KLF15 (Kruppel-like factor 15) controls plasma corticosteroid transport and inflammatory responses through direct transcriptional activation of Serpina6, which encodes corticosteroid binding globulin (CBG). Klf15-deficient mice have profoundly low CBG, reduced plasma corticosteroid binding capacity, and heightened mortality during inflammatory stress. These defects are completely rescued by reconstituting CBG, supporting that KLF15 works primarily through CBG to control plasma corticosterone homeostasis. To understand transcriptional mechanisms, we generated the first KLF15 cistromes using newly engineered Klf153xFLAG mice. Unexpectedly, liver KLF15 is predominantly promoter-enriched, including Serpina6, where it binds a palindromic GC-rich motif, opens chromatin, and transactivates genes with minimal associated gene repression. Overall, we provide new mechanistic insight into KLF15 function and identify a hepatocyte-intrinsic transcriptional module that potently regulates systemic corticosteroid transport and inflammation.

2021-12-28 | GSE166083 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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