Similar Datasets
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
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
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
Project description:Kruppel like factors (KLFs) are a subfamily of zinc finger proteins. As one of the family members, KLF15 can specifically bind to GC rich sequences on the promoter, thereby exerting transcriptional regulatory effects. Here we found that KLF15 negatively regulates angiogenesis in endothelial cells. KLF15 induces an increase in vasorin (VASN) expression, thereby activating the Notch signaling pathway and leading to a decrease in angiogenesis. These findings point to an KLF15/VASN axis as critical determinants of Notch signaling activation.
2025-05-24 | GSE287265 | GEO
Project description:Kruppel like factors (KLFs) are a subfamily of zinc finger proteins. As one of the family members, KLF15 can specifically bind to GC rich sequences on the promoter, thereby exerting transcriptional regulatory effects. Here we found that KLF15 negatively regulates angiogenesis in endothelial cells. KLF15 induces an increase in vasorin (VASN) expression, thereby activating the Notch signaling pathway and leading to a decrease in angiogenesis. These findings point to an KLF15/VASN axis as critical determinants of Notch signaling activation.
2025-05-24 | GSE287264 | GEO
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
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
Project description:Angiogenesis is a dynamic process fine-tuned by transcription factors in endothelial cells. The Krüpple-like factor 15 (KLF15)-mediated transcriptional regulation mechanism is critical for cardiovascular diseases. However, the role of endothelial KLF15 in governing angiogenesis remains unknown.KLF15 and vasorin (VASN) were deleted from endothelial cells using tamoxifen-inducible Cdh5-promoter-driven Cre recombinase in EC-KLF15 KO and EC-VASN KO mice, respectively. EC-KLF15 KO, EC-VASN KO and control mice were subjected to retinal angiogenesis or tumor cell transplantation. The RNA sequencing (RNA-seq), ATAC-seq, and ChIP-seq were conducted to identify VASN as a downstream effector of KLF15. Cell proliferation, wound healing, tube formation, and sprouting assays were performed to delineate endothelial cell function. In EC-KLF15 KO mice and adenovirus-mediated KLF15 overexpression mice, we showed that KLF15 negatively regulated retinal angiogenesis, as confirmed in cultured endothelial cells. KLF15 opened chromatin, bound to the promoters of GC-rich sequences, and transactivated the expression of VASN. Subsequently, VASN suppressed endothelial angiogenic function which was essential for Dll4-induced Notch1 signaling activation. Moreover, increased expression of VASN in EC-KLF15 KO mice suppressed retinal angiogenesis, which was attenuated by γ-secretase inhibitor. EC-VASN KO mice recapitulated the promotion of retinal angiogenesis in EC-KLF15 KO mice. Finally, the EGF-like domain of VASN was essential for its interaction with Notch1, and VASN EGF-like domain-derived peptides activated Notch1 signaling and suppressed angiogenesis.The KLF15/VASN axis negatively regulates angiogenesis by activating Notch1 signaling. KLF15 and VASN in endothelial cells might represent novel therapeutic targets for the treatment of impaired angiogenesis-related diseases and tumors.
2025-05-22 | GSE286440 | GEO
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
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