ArticlePloS one2009
Species-specific differences in the expression of the HNF1A, HNF1B and HNF4A genes.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Associations between Genotype-Diet Interactions and Weight Loss-A Systematic Review.Nutrients · 2020Pooled it
- Prognostic relevance of molecular subtypes and master regulators in pancreatic ductal adenocarcinoma.BMC cancer · 2016Trial
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- The metabolic dysfunction-associated steatohepatitis (MASH) drug resmetirom exhibits broad nuclear receptor activity with minimal functional impact.Scientific reports · 2026Article
- Quality control strategy for differentiating induced pluripotent stem cells into pancreatic β-cells before transplantation.Regenerative medicine · 2026Review
- Why all MODY variants in transcription factor genes are dominantly inherited.Frontiers in genetics · 2025Article
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- Machine-guided design of synthetic cell type-specificbioRxiv : the preprint server for biology · 2023Article
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- Pharmacological disruption of mSWI/SNF complex activity restricts SARS-CoV-2 infection.Nature genetics · 2023Article
- The protein architecture and allosteric landscape of HNF4α.Frontiers in endocrinology · 2023Review
- Multiple roles and regulatory mechanisms of the transcription factor HNF4 in the intestine.Frontiers in endocrinology · 2023Review
- HNF1A POU Domain Mutations Found in Japanese Liver Cancer Patients Cause Downregulation ofGenes · 2022Article
- Comprehensive quantitative analysis of alternative splicing variants reveals the HNF1B mRNA splicing pattern in various tumour and non-tumour tissues.Scientific reports · 2022Article
- HNF1A：From Monogenic Diabetes to Type 2 Diabetes and Gestational Diabetes Mellitus.Frontiers in endocrinology · 2022Review
- Modeling HNF1B-associated monogenic diabetes using human iPSCs reveals an early stage impairment of the pancreatic developmental program.Stem cell reports · 2021Article
- Maturity Onset Diabetes of the Young-New Approaches for Disease Modelling.International journal of molecular sciences · 2021Review
- Hepatocyte nuclear factor 1 beta: A perspective in cancer.Cancer medicine · 2021Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe HNF1A, HNF1B and HNF4A genes are part of an autoregulatory network in mammalian pancreas, liver, kidney and gut. The layout of this network appears to be similar in rodents and humans, but inactivation of HNF1A, HNF1B or HNF4A genes in animal models cause divergent phenotypes to those seen in man. We hypothesised that some differences may arise from variation in the expression profile of alternatively processed isoforms between species. METHODOLOGY/PRINCIPAL
findingsWe measured the expression of the major isoforms of the HNF1A, HNF1B and HNF4A genes in human and rodent pancreas, islet, liver and kidney by isoform-specific quantitative real-time PCR and compared their expression by the comparative Ct (DeltaDeltaCt) method. We found major changes in the expression profiles of the HNF genes between humans and rodents. The principal difference lies in the expression of the HNF1A gene, which exists as three isoforms in man, but as a single isoform only in rodents. More subtle changes were to the balance of HNF1B and HNF4A isoforms between species; the repressor isoform HNF1B(C) comprised only 6% in human islets compared with 24-26% in rodents (p = 0.006) whereas HNF4A9 comprised 22% of HNF4A expression in human pancreas but only 11% in rodents (p = 0.001). CONCLUSIONS/SIGNIFICANCE: The differences we note in the isoform-specific expression of the human and rodent HNF1A, HNF1B and HNF4A genes may impact on the absolute activity of these genes, and therefore on the activity of the pancreatic transcription factor network as a whole. We conclude that alterations to expression of HNF isoforms may underlie some of the phenotypic variation caused by mutations in these genes.
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