Project description:Histones were isolated from brown adipose tissue and liver from mice housed at 28, 22, or 8 C. Quantitative top- or middle-down approaches were used to quantitate histone H4 and H3.2 proteoforms. See published article for complimentary RNA-seq and RRBS datasets.
Project description:The first GSSM of V. vinifera was reconstructed (MODEL2408120001). Tissue-specific models for stem, leaf, and berry of the Cabernet Sauvignon cultivar were generated from the original model, through the integration of RNA-Seq data. These models have been merged into diel multi-tissue models to study the interactions between tissues at light and dark phases.
2024-09-02 | MODEL2408160001 | BioModels
Project description:RNA-Seq of WT and Tollip-KO mice liver
| PRJNA543694 | ENA
Project description:RNA-Seq of Flox and IRF6-HKO mice liver
Project description:We generated genome-wide cistromes of BAF180 subunit of the SWI-SNF chromatin remodeling complex in mouse liver at CT10 and CT22. In addition, we performed ChIP-Seq analysis on REV-ERBα in WT and SRC-2-/- mouse liver at CT10. We found circadian oscilation of BAF180 chromatin recruitment in mouse liver with peak recruitment at CT22 and nadir at CT10. Further,REV-ERBα chromatin recruitment was significantly reduced in SRC-2-/- mouse liver compared to WT mice at CT10. ChIP-Seq for BAF180 was performed in WT mice liver at CT10 and CT22 using two different antibodies. ChIP-Seq for REV-ERBα was performed in WT and SRC-2-/- mice in liver at CT10 with biological replicates.
Project description:Activation of protein kinase C epsilon (PKCε) in the liver has been widely associated with hepatic insulin resistance. PKCε is proposed to inhibit insulin signalling through phosphorylation of the insulin receptor. We have tested this directly by breeding PKCε floxed mice with mice expressing Cre recombinase under the control of the cytomegalovirus, albumin or adiponectin promoters to generate global, liver- and adipose tissue-specific PKCε knockout (KO) mice. Global deletion of PKCε recapitulated the benefits for diet-induced glucose intolerance that we previously described using conventional PKCε KO mice. However, we did not detect PKCε-dependent alterations in hepatic insulin receptor phosphorylation. Furthermore, liver-specific KO mice were not protected against diet-induced glucose intolerance or insulin resistance determined by euglycemic clamp. In contrast, adipose tissue-specific KO mice exhibited improved glucose tolerance and mildly increased hepatic triglyceride storage, but no change in liver insulin sensitivity. Phosphoproteomic analysis of insulin signalling in PKCε KO adipocytes revealed no defect in the canonical INSR/AKT/mTOR pathways. However, PKCε KO resulted in changes in phosphorylation of several proteins associated with the endosome and cell junctions suggesting regulation in secretory pathways and a potential role of PKCε in endocrine function. Indeed, RNA-seq analysis revealed adipose-tissue PKCε-dependent changes in the hepatic expression of several genes linked to glucose homeostasis and hepatic lipid metabolism. The primary effect of PKCε on glucose homeostasis is therefore not exerted directly in the liver as currently assumed. However, PKCε in adipose tissue modulates glucose tolerance and is involved in crosstalk with the liver that affects gene expression and lipid accumulation.
Project description:We futher characterized genome-wide chromatin accessibility of WT and SRC-2-/- mouse liver at CT10 through DNase-Seq. In addition,chromatin accessibility was significantly reduced in SRC-2-/- mouse liver compared to WT mice at CT10. DNase-Seq was carried out in WT and SRC-2-/- mice in liver at CT10 using two doses of DNaseI.