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Expression data from SOX9 overexpressing EndoC-ßH1 cells

ABSTRACT: Expression data from SOX9 overexpressing EndoC-ßH1 cells

PROVIDER: PRJNA412126 | ENA |

REPOSITORIES: ENA

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Expression data from SOX9 overexpressing EndoC-ßH1 cells

Project description:Human ß cell dedifferentiation as a potent mechanism of diabetes is gaining prominence. Several data suggest an upregulation of the transcription factor SOX9, a progenitor and duct cell marker during ß cell dedifferentiation. However, its targets in such cells need more understanding. Here, we overexpressed SOX9 and a constitutively active mutant (VP16-SOX9∆TAD) in Human pancreatic beta EndoC-ßH1 cells in order to understand its targets.

2018-01-31 | GSE104195 | GEO

Expression data from PolyIC treated EndoC-ßH1 cells

Project description:Type 1 diabetes (T1D) is a chronic disease characterized by an autoimmune-mediated destruction of insulin-producing pancreatic β cells. Environmental factors such as viruses play an important role in the onset of T1D and interact with predisposing genes. Recent data suggest that viral infection of human islets leads to a decrease in insulin production rather than β cell death, suggesting loss of β cell identity. We undertook this study to examine whether viral infection could induce human ß cell dedifferentiation. Using the functional human β cell line EndoC-βH1, we demonstrate that polyinosinic-polycitidilic acid (PolyI:C), a synthetic double-stranded RNA that mimics a by-product of viral replication induces a decrease in β cell-specific gene expression. In parallel to this loss, the expression of progenitor-like genes such as SOX9 was activated following PolyI:C treatment or enteroviral infection. SOX9 was induced by the NF-kB pathway and also in a paracrine non-cell autonomous fashion through the secretion of IFNA. Finally, we identified new SOX9 targets in human β cells as new markers of dedifferentiation in T1D. These findings reveal that inflammatory signaling has clear implications in human β cell dedifferentiation.

2018-01-31 | GSE104190 | GEO

Expression data from PolyIC treated EndoC-ßH1 cells

Project description:Expression data from PolyIC treated EndoC-ßH1 cells

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RNA-Sequencing of EndoC-BH1 cells Overexpressing OAS1, OAS2, or OAS3

Project description:RNA-Sequencing of EndoC-BH1 cells Overexpressing OAS1, OAS2, or OAS3

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

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RNA-Sequencing of EndoC-BH1 cells Overexpressing OAS1, OAS2, or OAS3

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2024-01-01 | GSE244273 | GEO

UMI-4C in control and HASTER-deficient EndoC-betaH3 cells overexpressing HNF1A

Project description:UMI-4C in control and HASTER-deficient EndoC-betaH3 cells overexpressing HNF1A

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Expression data from SOX9 knockdown in HCC cells

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UMI-4C in control and HASTER-deficient EndoC-betaH3 cells overexpressing HNF1A

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription HNF1A. If HASTER is deleted after beta cells have been formed and HNF1A is already stably expressed, HASTER is not required to maintain HNF1A activity, and is only required to provide negative feedback on HNF1A. HNF1A binding to the HASTER promoter mediates the repression of the HNF1A gene itself. To determine whether HNF1A binding to the HASTER promoter remodels 3D chromatin interactions of the HNF1A promoter, we performed UMI-4C experiments in wild type and HASTER-promoter KO EndoC-betaH3 cells with or without doxycycline-induced HNF1A overexpression using the HNF1A promoter as viewpoint.

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Expression data of Gyc76C overexpressing larvae

Project description:Expression data of Gyc76C overexpressing larvae

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