Project description:Studying the conservation and differences of regulation between human and mouse helps understand gene regulation on mouse models. Chromatin loop is an important gene regulatory mechanism to drive the 3D regulation between genes and their regulatory elements. Here, we performed eHi-C to profile genome wide contacts in mouse strains B6 and CAST islet beta cells, together with the loops identified in human islet alpha and beta cells from previous studies (GSE195523). The results show that the conserved chromation loop and open chromatin regions highlight the function of T2D risk loci and improve our understanding in islet biology.
Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with TGF-beta (transforming growth factor-beta) labeled with Cy5- time course with repeats Keywords: ordered
Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with Interferon-beta (IFN beta) labeled with Cy5- time course with repeats Keywords: ordered
Project description:Experimental Description<br><br>Mice overexpressing lymphotoxin alpha and beta, mice overexpressing lymphotoxin alpha and beta with concomitant hepatocyte-specific knock-out of the IKK-beta gene, and wild type C57BL/6 mice were sacrificed at 3 and 9 months of age, resp. From the respective livers, mRNA was extracted and whole genome transcription profiling was conducted with hybridization on day 1,2 or 3.
Project description:Primary cardiac fibroblasts were isolated from neonatal C57BL/6J mouse hearts and stimulated with TGF-β1 in vitro to induce a profibrotic phenotype. Bulk RNA sequencing was performed on fibroblasts treated with TGF-β for 48 hours and on matched untreated controls to characterize transcriptional programs associated with TGF-β–driven fibroblast activation. Differential expression and gene ontology analyses were used to identify pathways related to extracellular matrix remodeling, TGF-β signaling, and DNA damage responses. These data support mechanistic studies on CRABP2–MRE11–MRN–dependent regulation of cardiac fibroblast activation and fibrosis.
