Co Regulators Of Hepatocyte Nuclear Factor 4 Alpha Hnf4 Alpha
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Co Regulators of Hepatocyte Nuclear Factor 4 Alpha HNF4 Alpha
Author | : Yutaka Maeda |
Publsiher | : Unknown |
Total Pages | : 420 |
Release | : 2002 |
Genre | : Hepatocyte growth factor |
ISBN | : UCR:31210016751677 |
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Quantification of Hepatocyte Nuclear Factor 4 Alpha HNF4 alpha Protein in Liver
Author | : Joanna Irene Rosa Camba-Colón |
Publsiher | : Unknown |
Total Pages | : 294 |
Release | : 2005 |
Genre | : DNA-protein interactions |
ISBN | : UCR:31210019969953 |
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Hepatocyte Nuclear Factor 4alpha
Author | : Wendy Wenhua Hwang-Verslues |
Publsiher | : Unknown |
Total Pages | : 394 |
Release | : 2007 |
Genre | : Cell proliferation |
ISBN | : UCR:31210015196510 |
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Determinants of Cofactor Recruitment and Transcriptional Activity for Hepatocyte Nuclear Factor 4alpha HNF4alpha
Author | : Micheal Dean Ruse (Jr.) |
Publsiher | : Unknown |
Total Pages | : 398 |
Release | : 2002 |
Genre | : DNA-protein interactions |
ISBN | : UCR:31210016753285 |
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Hepatocyte Nuclear Factors Advances in Research and Application 2012 Edition
Author | : Anonim |
Publsiher | : ScholarlyEditions |
Total Pages | : 20 |
Release | : 2012-12-26 |
Genre | : Medical |
ISBN | : 9781481640626 |
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Hepatocyte Nuclear Factors—Advances in Research and Application: 2012 Edition is a ScholarlyPaper™ that delivers timely, authoritative, and intensively focused information about Hepatocyte Nuclear Factors in a compact format. The editors have built Hepatocyte Nuclear Factors—Advances in Research and Application: 2012 Edition on the vast information databases of ScholarlyNews.™ You can expect the information about Hepatocyte Nuclear Factors in this eBook to be deeper than what you can access anywhere else, as well as consistently reliable, authoritative, informed, and relevant. The content of Hepatocyte Nuclear Factors—Advances in Research and Application: 2012 Edition has been produced by the world’s leading scientists, engineers, analysts, research institutions, and companies. All of the content is from peer-reviewed sources, and all of it is written, assembled, and edited by the editors at ScholarlyEditions™ and available exclusively from us. You now have a source you can cite with authority, confidence, and credibility. More information is available at http://www.ScholarlyEditions.com/.
Regulation of HNF4 Aplha Function by Phosphorylation and Protein protein Interaction
Author | : Kai Sun |
Publsiher | : Unknown |
Total Pages | : 334 |
Release | : 2005 |
Genre | : Hepatocyte growth factor |
ISBN | : UCR:31210021026909 |
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The Essential Fatty Acid Linoleic Acid is the Endogenous Ligand for the Orphan Nuclear Receptor Hepatocyte Nuclear Factor 4 Aplha
Author | : Tuong Chi Ta |
Publsiher | : Unknown |
Total Pages | : 510 |
Release | : 2009 |
Genre | : Cell receptors |
ISBN | : UCR:31210023258260 |
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Repression of HNF4A Enables Transcriptomic Reprogramming During the Hepatic Acute phase Response
![Repression of HNF4A Enables Transcriptomic Reprogramming During the Hepatic Acute phase Response](https://youbookinc.com/wp-content/uploads/2024/06/cover.jpg)
Author | : Charlotte Ehle |
Publsiher | : Unknown |
Total Pages | : 0 |
Release | : 2024* |
Genre | : Electronic Book |
ISBN | : OCLC:1436705459 |
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The hepatic acute-phase response is characterized by a massive upregulation of serum proteins, such as haptoglobin and serum amyloid A, at the expense of liver homeostatic functions. Although the transcription factor hepatocyte nuclear factor 4 alpha (HNF4A) has a well-established role in safeguarding liver function and its cistrome spans around 50% of liver-specific genes, its role in the acute-phase response has received little attention so far. We demonstrate that HNF4A binds to and represses acute-phase genes under basal conditions. The reprogramming of hepatic transcription during inflammation necessitates loss of HNF4A function to allow expression of acute-phase genes while liver homeostatic genes are repressed. In a pre-clinical liver organoid model overexpression of HNF4A maintained liver functionality in spite of inflammation-induced cell damage. Conversely, HNF4A overexpression potently impaired the acute-phase response by retaining chromatin at regulatory regions of acute-phase genes inaccessible to transcription. Taken together, our data extend the understanding of dual HNF4A action as transcriptional activator and repressor, establishing HNF4A as gatekeeper for the hepatic acute-phase response.