Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome profile of INS-1E Ctrl and hTFEB OE cells

ABSTRACT: To analyse gene expression differences between the human TFEB overexpressing cells vs. Controls, under growing conditions (GC) vs. Fasting conditions (Fast)

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE155221 | GEO | 2023/07/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome profile of INS-1E Ctrl and DKO cells

Project description:To analyse gene expression differences between the TFEB/TFE3 KO cells vs. Controls, under growing conditions (GC) vs. Fasting conditions (Fast)

2023-07-31 | GSE153709 | GEO

Transcriptome profile of ENDOC-BH1 cells overexpressing TFEB-V5 or controls

Project description:To analyse gene expression differences between the TFEB overexpressing cells vs. Controls, under growing conditions (GC) vs. Fasting conditions (Fast).

2023-07-31 | GSE154059 | GEO

Transcriptome profile of ENDOC-BH1 cells silencing TFEB and TFE3 (siTFEB/TFE3) or controls

Project description:To analyze gene expression differences between cells silenced for TFEB and TFE3 vs. Controls, under growing conditions (GC) vs. Fasting conditions (Fast)

2023-07-31 | GSE155220 | GEO

Transcriptome profile of isolated murine islets overexpressing TFEB or controls

Project description:To analyse gene expression differences between the TFEB overexpressing islets vs. Controls.

2023-07-31 | GSE154062 | GEO

Expression data from rat INS-1E cells

2012-12-14 | GSE42897 | GEO

Expression data from rat INS-1E cells

Project description:Cytokine-induced beta-cell apoptosis is a key event for the death of pancreatic beta cells in the development of type-1 diabetes. We identified BRD0476 as a novel suppressor of cytokine-induced beta-cell apoptosis. We used microarrays to look for gene set(s) that are regulated by BRD0476. Rat INS-1E cells were treated with cytokine cocktails (IL-1b, IFN-g and TNF-a) and/or BRD0476 for 6 or 12 hours. Total RNAs were isolated using the RNEasy kit from Qiagen.

2012-12-14 | E-GEOD-42897 | biostudies-arrayexpress

Data of intracellular insulin protein reduced by autophagy in INS-1E cells.

Project description:Autophagy appears to be involved in maintaining normal intracellular insulin content by accelerating the insulin degradation rate in ?-cells (Marsh et al., 2007) [1]. 2-deoxy-d-glucose (2-DG) is metabolized by hexokinase, and acts as an inhibitor of glycolysis. 2-DG triggers glucose deprivation without altering other nutrients or metabolic pathways (Aghaee et al., 2012) [2], and appears to be an ideal tool for studying autophagy. Rapamycin induced upregulation of autophagy in both cultured isolated islets and pancreatic ?-cells (Tanemura et al., 2012) [3]. Here, we examined that 2-DG or rapamycin-induced autophagy may decrease the production of intracellular insulin in INS-1E insulinoma cells. Data showed that autophagy was increased by 2-DG or rapamycin by Western blotting and Immunofluorescence staining analyses. Also, intracellular insulin decreased by 2-DG or rapamycin. Furthermore, the autophagy inhibitors, bafilomycin A1 and/or 3-methyladenine, in the presence or absence of 2-DG or rapamycin increased intracellular insulin in INS-1E insulinoma cells.

| S-EPMC4976643 | biostudies-literature

Interactome of Ca2+-bound secretagogin in INS-1E cells

Project description:By using His6-tagged recombinant human secretagogin in the presence of Ca2+ (100 µM), we precipitated putative interacting partners from INS-1E cells and identified their amino acid sequences by mass spectrometry. We detected canonical interacting proteins participating in vesicle-mediated transport, exocytosis and cytoskeletal organization. Besides, we captured proteins controlling protein folding and (de-)ubiquitination. Our data support that secretagogin modulates protein folding and degradation through protein-protein interactions and interacts with USP9X in β cells to control cell survival.

2017-06-21 | PXD006544 | Pride

Transcriptome profile of RCS WT and TFEB/3 DKO cells transfected with mutant COL2R789C compared to control

Project description:To analyse gene expression differences between RCS COL2R789C transfected cells WT and TFEB/3 DKO compared to their relative scramble controls

2024-06-11 | GSE239527 | GEO

Overexpression of native IF1 downregulates glucose-stimulated insulin secretion by pancreatic INS-1E cells.

Project description:We have previously reported that transient knock-down of ATPase inhibitory factor 1 (IF1) by siRNA upregulates ATP levels and subsequently augments insulin secretion in model pancreatic ?-cells INS-1E. Here we investigated how long-term IF1-overexpression impacts pancreatic ?-cell bioenergetics and insulin secretion. We generated INS-1E cell line stably overexpressing native IF1. We revealed that IF1 overexpression leads to a substantial decrease in ATP levels and reduced glucose-stimulated insulin secretion. A decrease in total cellular ATP content was also reflected in decreased free ATP cytosolic and mitochondrial levels, as monitored with ATeam biosensor. Consistently, cellular respiration of IF1-overexpressing cells was decreased. 3D structured illumination microscopy (SIM) revealed a higher amount of insulin granules with higher volume in IF1-overexpressing cells. Similar effects occurred when cells were incubated at low glucose concentrations. Noteworthy, activation of PKA by dibutyryl cAMP entirely abolished the inhibitory effect of IF1 overexpression on ATP production and insulin secretion. Mitochondrial network morphology and cristae ultrastructure in INS-1E overexpressing IF1 remained mostly unchanged. Finally, we show that INS-1E cells decrease their IF1 protein levels relative to ATP synthase ?-subunit in response to increased glucose. In conclusion, IF1 actively downregulates INS-1E cellular metabolism and reduces their ability to secrete insulin.

| S-EPMC6994519 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data