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

ABSTRACT: 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. Keywords: comparative expression analysis, fasted state

ORGANISM(S): Mus musculus

PROVIDER: GSE7137 | GEO | 2007/04/02

SECONDARY ACCESSION(S): PRJNA98205

REPOSITORIES: GEO

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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

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Mus musculus

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

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KLF15

Project description:KLF15

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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.

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