A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation

The fundamental question of which genes are most important in controlling liver regeneration remains unanswered. We employed a parallel screen to test the impact of 43 selected genes on liver repopulation in the Fah(−/−) mouse model of hereditary tyrosinemia. We discovered that the transcription fac...

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Detalles Bibliográficos
Autores principales: Wangensteen, Kirk J., Zhang, Sophia, Greenbaum, Linda E., Kaestner, Klaus H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory Press 2015
Materias:
Research Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4421979/
https://www.ncbi.nlm.nih.gov/pubmed/25934503
http://dx.doi.org/10.1101/gad.258855.115
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author Wangensteen, Kirk J.
Zhang, Sophia
Greenbaum, Linda E.
Kaestner, Klaus H.
author_facet Wangensteen, Kirk J.
Zhang, Sophia
Greenbaum, Linda E.
Kaestner, Klaus H.
author_sort Wangensteen, Kirk J.
collection PubMed
description The fundamental question of which genes are most important in controlling liver regeneration remains unanswered. We employed a parallel screen to test the impact of 43 selected genes on liver repopulation in the Fah(−/−) mouse model of hereditary tyrosinemia. We discovered that the transcription factor Foxa3 was a strong promoter of liver regeneration, while tumor necrosis factor receptor 1 (TNFR1) was the most significant suppressor of repopulation among all of the genes tested. Our approach enabled the identification of these factors as important regulators of liver repopulation and potential drug targets for the promotion of liver repopulation.
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spelling pubmed-44219792015-11-01 A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation Wangensteen, Kirk J. Zhang, Sophia Greenbaum, Linda E. Kaestner, Klaus H. Genes Dev Research Communication The fundamental question of which genes are most important in controlling liver regeneration remains unanswered. We employed a parallel screen to test the impact of 43 selected genes on liver repopulation in the Fah(−/−) mouse model of hereditary tyrosinemia. We discovered that the transcription factor Foxa3 was a strong promoter of liver regeneration, while tumor necrosis factor receptor 1 (TNFR1) was the most significant suppressor of repopulation among all of the genes tested. Our approach enabled the identification of these factors as important regulators of liver repopulation and potential drug targets for the promotion of liver repopulation. Cold Spring Harbor Laboratory Press 2015-05-01 /pmc/articles/PMC4421979/ /pubmed/25934503 http://dx.doi.org/10.1101/gad.258855.115 Text en © 2015 Wangensteen et al.; Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by-nc/4.0/ This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.
spellingShingle Research Communication
Wangensteen, Kirk J.
Zhang, Sophia
Greenbaum, Linda E.
Kaestner, Klaus H.
A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation
title A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation
title_full A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation
title_fullStr A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation
title_full_unstemmed A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation
title_short A genetic screen reveals Foxa3 and TNFR1 as key regulators of liver repopulation
title_sort genetic screen reveals foxa3 and tnfr1 as key regulators of liver repopulation
topic Research Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4421979/
https://www.ncbi.nlm.nih.gov/pubmed/25934503
http://dx.doi.org/10.1101/gad.258855.115
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