TCF19 Impacts a Network of Inflammatory and DNA Damage Response Genes in the Pancreatic β-Cell
Autor: | Sukanya Lodh, Avtar Roopra, Grace H. Yang, Danielle A. Fontaine, Joseph T. Blumer, Dawn Belt Davis |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
DNA damage Endocrinology Diabetes and Metabolism Cell Inflammation Biology Biochemistry Microbiology Article 03 medical and health sciences 0302 clinical medicine Gene expression medicine PANTHER TCF19 Molecular Biology Gene Transcription factor Gene knockdown diabetes STRING QR1-502 β-cell Cell biology 030104 developmental biology medicine.anatomical_structure Apoptosis inflammation 030220 oncology & carcinogenesis medicine.symptom RNA-seq |
Zdroj: | Metabolites Volume 11 Issue 8 Metabolites, Vol 11, Iss 513, p 513 (2021) |
ISSN: | 2218-1989 |
DOI: | 10.3390/metabo11080513 |
Popis: | Transcription factor 19 (TCF19) is a gene associated with type 1 diabetes (T1DM) and type 2 diabetes (T2DM) in genome-wide association studies. Prior studies have demonstrated that Tcf19 knockdown impairs β-cell proliferation and increases apoptosis. However, little is known about its role in diabetes pathogenesis or the effects of TCF19 gain-of-function. The aim of this study was to examine the impact of TCF19 overexpression in INS-1 β-cells and human islets on proliferation and gene expression. With TCF19 overexpression, there was an increase in nucleotide incorporation without any change in cell cycle gene expression, alluding to an alternate process of nucleotide incorporation. Analysis of RNA-seq of TCF19 overexpressing cells revealed increased expression of several DNA damage response (DDR) genes, as well as a tightly linked set of genes involved in viral responses, immune system processes, and inflammation. This connectivity between DNA damage and inflammatory gene expression has not been well studied in the β-cell and suggests a novel role for TCF19 in regulating these pathways. Future studies determining how TCF19 may modulate these pathways can provide potential targets for improving β-cell survival. |
Databáze: | OpenAIRE |
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