Beta-cell_CaMPARI
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB64493 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Single-cell transcriptome profiling of zebrafish pancreatic beta-cells segregated by CaMPARI-based calcium labeling.
| PRJNA996961 | ENA
Project description:To better understand the underlying mechanism of beta-cell regeneration in adult zebrafish, we performed single-cell transcriptomic profiling of the pancreatic tissue (using 10X Genomics) at various stages post beta-cell ablation.
2022-06-21 | GSE166052 | GEO
Project description:Redox signaling mediated by reversible oxidative cysteine thiol modifications is crucial for driving cellular adaptation to dynamic environmental changes, maintaining homeostasis, and ensuring proper function. This is particularly critical in pancreatic β-cells, which are highly metabolically active and play a specialized role in whole organism glucose homeostasis. Glucose stimulation in β-cells triggers signals leading to insulin secretion, including changes in ATP/ADP ratio and intracellular calcium levels. Additionally, lipid metabolism and reactive oxygen species (ROS) signaling are essential for β-cell function and health. We employed IodoTMT isobaric labeling combined with tandem mass spectrometry to elucidate redox signaling pathways in pancreatic β-cells.
2024-09-30 | PXD052765 | Pride
Project description:In this study, we generated a novel nuclear-localized red fluorescence knock-in reporter allele (Ins2.Apple) for mouse pancreatic beta-cells. Beta-cells were isolated by FACS from 60-day-old mice, segregated by sex, and RNA-sequencing was performed to assess sex-specific differences in beta-cell gene expression profiles. We also isolated beta-cells (by FACS) from MIP-GFP mice at 60 days of age. RNA-sequencing was performed, and was compared to that of Ins2.Apple beta cells, to assess gene expression changes brought on by the presence of the MIP-GFP transgene.
2018-12-15 | E-MTAB-6329 | biostudies-arrayexpress
Project description:Autophagy plays an important role in preserving cellular homeostasis in pancreatic beta cells. However, the extent of autophagic flux induced in various physiological settings in vivo is unclear. In this study, we generated transgenic mice expressing pHluorin-LC3-mCherry reporter for monitoring systemic autophagic flux. Our findings revealed that autophagic flux in pancreatic islets enhanced after starvation, although suppression of the flux after short-term refeeding needs more prolonged restarvation in islets than in liver and skeletal muscle. Furthermore, heterogeneity of autophagic flux in beta cells manifested after increasing insulin resistance and intracellular calcium influx by glucose stimulation increased more in high- than low-flux beta cells, with differential gene expression based on the flux. Thus, our monitor mouse enables us to reveal physiological response and biological insight of heterogeneity in autophagic flux in pancreatic beta cells.
2023-03-15 | PXD036390 | JPOST Repository
Project description:DEAD-box helicase 1 (DDX1) is a multifunction protein involved in diverse cellular processes including transcription, viral replication, mRNA/miRNA processing, and tRNA splicing. Here, we report a novel function of DDX1 in mRNA alternative splicing in pancreatic β cells. By performing integrated data analysis of high-throughput RNA sequencing (RNA-Seq), and cross-linking and immunoprecipitation coupled with deep sequencing (CLIP-Seq), we identify hundreds of alternative splicing genes that are targeted by DDX1. These DDX1-targeted alternative splicing genes are mainly associated with calcium ion binding, high voltage-gated calcium channel, and transmembrane transporter. Functionally, silencing DDX1 impairs calcium influx and insulin secretion in the pancreatic β cells. These results reveal an important role for DDX1 in the regulation of gene alternative splicing and insulin secretion in pancreatic β cells.
2018-05-02 | GSE113893 | GEO
Project description:Pancreatic beta-calls are responsible for regulating the blood glucose levels via secretion of hormone insulin. To elucidate the chromatin state in zebrafish beta-cells, we performed ATAC-Sequencing.
2021-12-31 | GSE152199 | GEO
Project description:ATAC sequencing of zebrafish pancreatic beta-cells
| PRJNA638621 | ENA
Project description:Pancreatic beta cells use electrical signals to couple changes in blood glucose concentration to insulin release via extracellular calcium (Ca2+) influx. Sorcin (SRI) is a Ca2+-binding protein whose overexpression in cardiomyocytes rescues the abnormal contractile function of the diabetic heart. In order to investigate the role of sorcin in regulating mouse pancreatic beta cell transcriptome, transgenic mice were generated on a C56BL/6 background permitting inducible overexpression of SRI cDNA with the TetOn-system specifically in beta cells. Animals bearing ten copies of the SRI transgene (SRI-tg10), and littermate controls, were fed a high fat diet (60% fat, HFD) and exposed to doxycycline in the drinking water (500mg/L) from 4 weeks onwards. Microarray analysis were performed using total RNA from isolated pancreatic islets of 8-week-old mice.
2015-09-09 | E-GEOD-72719 | biostudies-arrayexpress
Project description:Objective: Redox signaling mediated by reversible oxidative cysteine thiol modifications is crucial for driving cellular adaptation to dynamic environmental changes, maintaining homeostasis, and ensuring proper function. This is particularly critical in pancreatic β-cells, which are highly metabolically active and play a specialized role in whole organism glucose homeostasis. Glucose stimulation in β-cells triggers signals leading to insulin secretion, including changes in ATP/ADP ratio and intracellular calcium levels. Additionally, lipid metabolism and reactive oxygen species (ROS) signaling are essential for β-cell function and health. Methods: We employed IodoTMT isobaric labeling combined with tandem mass spectrometry to elucidate redox signaling pathways in pancreatic β-cells. Results: Glucose stimulation significantly increases ROS levels in β-cells, leading to targeted reversible oxidation of proteins involved in key metabolic pathways such as glycolysis, the tricarboxylic acid (TCA) cycle, pyruvate metabolism, oxidative phosphorylation, protein processing in the endoplasmic reticulum (ER), and insulin secretion. Furthermore, the glucose-induced increase in reversible cysteine oxidation correlates with the presence of other post-translational modifications, including acetylation and phosphorylation. Conclusions: Proper functioning of pancreatic β-cell metabolism relies on fine-tuned regulation, achieved through a sophisticated system of diverse post-translational modifications that modulate protein functions. Our findings demonstrate that glucose induces the production of ROS in pancreatic β-cells, leading to targeted reversible oxidative modifications of proteins. Furthermore, protein activity is modulated by acetylation and phosphorylation, highlighting the complexity of the regulatory mechanisms in β-cell function.
2024-09-15 | GSE274980 | GEO