Project description:To investigate the function of MAFB in the regulation of human beta cell identity and maturity, we established EndoCbH2 cell lines in which MAFB has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from bulkRNA-seq of 3 biological replicates.
Project description:We deposit the data of single-cell and bulk-cell rna-seq of normal mouse heart. In addition, we conducted bulk rna-seq in human sample and found that many of the heart remodelling-associated genes we discovered show conserved expression pattern in human hypertrophy and heart failure stage.
Project description:By comprehensive screening of long non-coding RNAs (lncRNAs) over mouse heart development, we have identified Tbx5 upstream antisense RNA (Tbx5ua). In order to understand its function, we produced Tbx5ua knock down ES cells by inserting triple bovine polyadenylation signal to the second exon of Tbx5ua. From the ES cells we made chimeric mouse embryos via tetraploid complementation assay. We conducted RNA-seq analysis on the WT and KD heart ventricles at E9.5 to further elucidate the lncRNA's molecular functions.
Project description:This database provides TMT-labeled proteomic data of aorta (thoracic aorta), brain, heart, kidney, liver, lung, muscle (gastrocnemius muscle), and skin (abdominal skin) of 6, 15, 24, and 30 months old male C57BL/6 mice. In addition to the whole-tissue lysate, low-soluble protein-enriched fraction was also analyzed for heart, kidney, lung, muscle, and skin. Bulk RNA-Seq data are available for brain, heart, kidney, liver, lung, muscle, and skin. The tissues used for transcriptomic analysis and proteomic analysis of whole-tissue lysate and low-soluble protein-enriched fraction were collected from the same mice. All analyses were conducted with 4 biological replicates.
Project description:Recently, we found that human TNF transgenic (TNF-Tg) mice died by 6-month from cardiopulmonary disease. Histological analysis showed that TNF-Tg mice were characterized by the pulmonary vascular and right ventricular pathology. This pathology closely mimics human connective tissue disease (CTD) associated pulmonary arterial hypertension (PAH). In this study, we aimed to investigate the gene expression in TNF-Tg lung using bulkRNA-seq technology.
Project description:In this project, we conducted an evaluation of mass spectrometry methods using mouse heart and HCT116 cell samples. The results demonstrated that the data-independent acquisition (DIA) approach outperformed data-dependent acquisition (DDA) in the identification of Altprot and canonical proteins. Subsequently, we assessed several different DIA library building methods, including traditional DDA-based library building, gas-phase fractionation(GPF) library building, and machine learning-based prediction library building. Notably, the traditional DDA library building method exhibited a higher likelihood of false positive identifications. Furthermore, we applied the aforementioned mass spectrometry methods to investigate the process of mouse heart development. Through this analysis, we identified a subset of Altprots, including ASDURF, which may potentially play crucial roles in heart development. These findings serve as a fundamental basis for future exploration and investigation of Altprot in this context.
Project description:The abberant resurgence of which have been recently found to link to some critical pathologies. To evaluate the occurrence and role of ERV resurrgenece in heart and heart failure (HF), we conducted heart total RNA-seq analysis from mice ischemia-reperfusion (I/R) heart failure models and found that ERVs were activated which is similar in various cross-species models of heart failure. To explore the mechanism of ERVs resurgence we profiled trimethylation at lysine 9 of histone H3 (H3K9me3) ChIP- and MeRIP-seq of cardiomyocytes specific TRIM28 knockout mice heart. The deprivation of TRIM28 in the mouse myocardium attenuated the epigenetic surveillance of H3K9me3 and N6-methyladenosine (m6A), and revived the ERVs, which consequently activated the intracellular antiviral innate immune pathways of TLR7-9 and NF-kappaB and lead to the myocarditis and acute heart failure.