ArticleAmerican journal of physiology. Endocrinology and metabolism2013
Tcf19 is a novel islet factor necessary for proliferation and survival in the INS-1 β-cell line.
Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Transcriptome-wide association study of multiple myeloma identifies candidate susceptibility genes.Human genomics · 2019Pooled it
- Genome-Wide Association Study of Psoriasis, Psoriatic Arthritis, Anti-TNF-α Response, and Polygenic Risk Score in a Russian Cohort.International journal of molecular sciences · 2026Article
- Emerging Role of Transcription Factor 19 (TCF19) in Inflammatory Disease and Cancer.Biomolecules · 2026Review
- Exploratory transcriptomics andBiomedical reports · 2026Article
- TCF19 promotes gastric cancer progression through MCM6.BMC gastroenterology · 2025Article
- A bioinformatics screen identifies TCF19 as an aggressiveness-sustaining gene in prostate cancer.Molecular oncology · 2025Article
- Downregulation of TCF19 and ATAD2 causes endothelial cell cycle arrest at the transition from cardiac hypertrophy to heart failure.Basic research in cardiology · 2025Article
- The upregulation of GDF15 is controlled epigenetically by oncogenic TCF19 signaling in human hepatocellular carcinoma.iScience · 2025Article
- TCF19 drives a broad transcriptional program that potentiates optimal innate and adaptive functions of antiviral NK cells.Nature immunology · 2025Article
- TCF19 expression and significance analysis in breast cancer: integrated bioinformatics analysis and histological validation.Discover oncology · 2025Article
- Improving T2D machine learning-based prediction accuracy with SNPs and younger age.Computational and structural biotechnology journal · 2025Article
- TCF19 Enhances Glioma Cell Proliferation via Modulating the Β-Catenin Signaling Pathway through Accelerating DHX32 Transcription.Current cancer drug targets · 2025Article
- Article
- Review
- Cell cycle regulation of the psoriasis associated gene CCHCR1 by transcription factor E2F1.PloS one · 2023Article
- Epigenetic Reprogramming of the Glucose Metabolic Pathways by the Chromatin Effectors During Cancer.Sub-cellular biochemistry · 2022Article
- Immunotherapeutic Value of Transcription Factor 19 (TCF19) Associated with Renal Clear Cell Carcinoma: A Comprehensive Analysis of 33 Human Cancer Cases.Journal of oncology · 2022Article
- Exon and intron sharing in opposite direction-an undocumented phenomenon in human genome-between Pou5f1 and Tcf19 genes.BMC genomics · 2021Article
- Prostaglandin EP3 receptor signaling is required to prevent insulin hypersecretion and metabolic dysfunction in a non-obese mouse model of insulin resistance.American journal of physiology. Endocrinology and metabolism · 2021Article
- In Silico Analysis to Explore Lineage-Independent and -Dependent Transcriptional Programs Associated with the Process of Endothelial and Neural Differentiation of Human Induced Pluripotent Stem Cells.Journal of clinical medicine · 2021Article
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Authors and funding
12 authors at 2 institutions in 1 country.
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Abstract
Recently, a novel type 1 diabetes association locus was identified at human chromosome 6p31.3, and transcription factor 19 (TCF19) is a likely causal gene. Little is known about Tcf19, and we now show that it plays a role in both proliferation and apoptosis in insulinoma cells. Tcf19 is expressed in mouse and human islets, with increasing mRNA expression in nondiabetic obesity. The expression of Tcf19 is correlated with β-cell mass expansion, suggesting that it may be a transcriptional regulator of β-cell mass. Increasing proliferation and decreasing apoptotic cell death are two strategies to increase pancreatic β-cell mass and prevent or delay diabetes. siRNA-mediated knockdown of Tcf19 in the INS-1 insulinoma cell line, a β-cell model, results in a decrease in proliferation and an increase in apoptosis. There was a significant reduction in the expression of numerous cell cycle genes from the late G1 phase through the M phase, and cells were arrested at the G1/S checkpoint. We also observed increased apoptosis and susceptibility to endoplasmic reticulum (ER) stress after Tcf19 knockdown. There was a reduction in expression of genes important for the maintenance of ER homeostasis (Bip, p58(IPK), Edem1, and calreticulin) and an increase in proapoptotic genes (Bim, Bid, Nix, Gadd34, and Pdia2). Therefore, Tcf19 is necessary for both proliferation and survival and is a novel regulator of these pathways.
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