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RNA Sequencing Facilitates Quantitative Analysis of Albumin-Cre (Control, Ctl) and Liver-specific Klf15 Knockout (Li-KO) Mouse Liver Transcriptomes

ABSTRACT: The goals of this study are to compare control and liver Klf15 deficient mouse liver transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis

ORGANISM(S): Mus musculus

PROVIDER: GSE126762 | GEO | 2019/02/22

REPOSITORIES: GEO

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RNA Sequencing Facilitates Quantitative Analysis of Albumin-Cre (Control, Ctl) and Liver-specific Klf15 Knockout (Li-KO) Mouse Liver Transcriptomes

Project description:RNA Sequencing Facilitates Quantitative Analysis of Albumin-Cre (Control, Ctl) and Liver-specific Klf15 Knockout (Li-KO) Mouse Liver Transcriptomes

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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

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

2007-04-02 | GSE7137 | 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

Comparison of glucocorticoid receptor (NR3C1) binding in wild type and Klf15-/- MEFs

Project description:The objective of this study was to dertemine GR binding patterns within wild type murine embryonic fibroblasts in comparison to embryonic fibroblasts derived from mice containing a null mutation for Klf15. This study utilized duplicate samples and the following conditions. Wild type cells treated with ethanol (pooled single sample secondary to low starting material); wild type cells treated with dexamethasone for 1 hour (2 samples); Klf15-/- cells treated with ethanol (2 samples); Klf15 -/- cells treated with dexamethasone (2 samples). Samples treated with ethanol served as controls.

2015-06-18 | E-GEOD-69947 | biostudies-arrayexpress

KLF15 dependent REV-ERBa binding in the heart

Project description:By comparing the ChIPseq signal of REV_ERBa in control (Flox) and cardiomyocytic KLF15 knockout (cKO), we identified the KLF15 dependent REV-ERBa binding and repression in the heart. We further compared the differential binding sites to KLF15 binding site, using a FLAG tagged cardiomyocytic transgenic (cTG1) mice.

2015-12-30 | GSE73741 | GEO

Expression data from 18h-fasted WT versus KLF15-null mice: heart

Project description:We used microarray analysis to identify differences in gene expression levels in heart following an 18h (overnight) fast in WT control and KLF15-null mice Heart tissue was isolated from 3-4 month old, 18h-fasted WT and KLF15-null male mice for RNA extraction and hydridization on Affymetrix microarrays

2014-01-09 | E-GEOD-53231 | biostudies-arrayexpress

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

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