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Title: The molecular functions of hepatocyte nuclear factors - in and beyond the liver
Authors: Lau, Hwee Hui
Ng, Natasha Hui Jin
Loo, Larry Sai Weng
Joanita Jasmen
Teo, Adrian Kee Keong
Keywords: Science::Medicine
Issue Date: 2018
Source: Lau, H. H., Ng, N. H. J., Loo, L. S. W., Joanita Jasmen., & Teo, Adrian K. K. (2018). The molecular functions of hepatocyte nuclear factors - in and beyond the liver. Journal of hematology, 68(5), 1033-1048. doi:10.1016/j.jhep.2017.11.026
Journal: Journal of hepatology
Abstract: The hepatocyte nuclear factors (HNFs) namely HNF1α/β, FOXA1/2/3, HNF4α/γ and ONECUT1/2 are expressed in a variety of tissues and organs, including the liver, pancreas and kidney. The spatial and temporal manner of HNF expression regulates embryonic development and subsequently the development of multiple tissues during adulthood. Though the HNFs were initially identified individually based on their roles in the liver, numerous studies have now revealed that the HNFs cross-regulate one another and exhibit synergistic relationships in the regulation of tissue development and function. The complex HNF transcriptional regulatory networks have largely been elucidated in rodent models, but less so in human biological systems. Several heterozygous mutations in these HNFs were found to cause diseases in humans but not in rodents, suggesting clear species-specific differences in mutational mechanisms that remain to be uncovered. In this review, we compare and contrast the expression patterns of the HNFs, the HNF cross-regulatory networks and how these liver-enriched transcription factors serve multiple functions in the liver and beyond, extending our focus to the pancreas and kidney. We also summarise the insights gained from both human and rodent studies of mutations in several HNFs that are known to lead to different disease conditions.
ISSN: 0168-8278
DOI: 10.1016/j.jhep.2017.11.026
Rights: © 2017 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
Fulltext Permission: none
Fulltext Availability: No Fulltext
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