Pancreatic β-cell specific Ets-1 inhibition treats type 2 diabetes via revitalized insulin production
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ABSTRACT:
PROVIDER: PRJNA887749 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21824839_1.fastq.gz | Fastqsanger.gz | |||
| SRR21824839_2.fastq.gz | Fastqsanger.gz | |||
| SRR21824840_1.fastq.gz | Fastqsanger.gz | |||
| SRR21824840_2.fastq.gz | Fastqsanger.gz | |||
| SRR21824841_1.fastq.gz | Fastqsanger.gz |
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Project description:As a transcription factor, Ets1 (E26 transformation-specific-1 transcription factor) plays an important role in cell growth, development, differentiation, etc. Our research found that it plays an crucial role in β cell dysfunction induced by metabolic stress such as high glucose. In order to further clarify the downstream target molecules of Ets1 in β cells and the potential mechanism of regulating the mRNA level of target molecules, we transfected Min6(Mouse insulinoma cells) with control virus (Ad-GFP) and Ets-1 overexpression adenovirus (Ad-Ets-1) respectively. Through immunoprecipitation of Ets1 antibody, the DNA fragment specifically bound to Ets1 was obtained and used in high-throughput sequencing. By comparing the enriched DNA fragment with mouse genome (mm10) DNA, the downstream genes that Ets1 can bind to under physiological conditions and the differential peak related genes after overexpression of Ets1 were obtained. Through GO analysis and KFGG analysis of the above related genes, it was confirmed that there was an obvious regulatory relationship between Ets1 and β cell function related genes. Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for E26 transformation-specific-1 transcription factor (Ets-1) in Min6 cells transfected Control virus (Ad-GFP) and Ets-1 overexpression adenovirus (Ad-Ets-1)
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