ArticleNucleic acids research2022
Decoding YAP dependent transcription in the liver.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- A YAP-TEAD-CTCF Transcriptional Regulatory Axis Associated With the Elimination of Injured Hepatocytes From the Liver.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Creatine metabolism regulates trophectoderm formation in early mouse embryos via an energy-cytoskeleton-YAP axis.The Journal of biological chemistry · 2026Article
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
- Nuclear Mechanotransduction at the Crossroads: How Membrane Receptors Remodel the Perinuclear Cytoskeleton to Drive Cancer and Disease.International journal of biological sciences · 2026Review
- Disrupting bile acid metabolism by suppressing Fxr causes hepatocellular carcinoma induced by YAP activation.Nature communications · 2025Article
- Review
- Targeting BRD4 mitigates hepatocellular lipotoxicity by suppressing the NLRP3 inflammasome activation and GSDMD-mediated hepatocyte pyroptosis.Cellular and molecular life sciences : CMLS · 2024Article
- Mitochondrial stress activates YAP/TAZ through RhoA oxidation to promote liver injury.Cell death & disease · 2024Article
- Aberrant MET activation impairs perinuclear actin cap organization with YAP1 cytosolic relocation.Communications biology · 2023Article
- Article
- Normalization of hepatic ChREBP activity does not protect against liver disease progression in a mouse model for Glycogen Storage Disease type Ia.Cancer & metabolism · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional coactivator YAP is emerging as a master regulator of cell growth. In the liver, YAP activity is linked to hepatomegaly, regeneration, dedifferentiation, and aggressive tumor growth. Here we present genomic studies to address how YAP may elicit such profound biological changes in murine models. YAP bound the genome in a TEAD-dependent manner, either at loci constitutively occupied by TEAD or by pioneering enhancers, which comprised a fraction of HNF4a/FOXA-bound embryonic enhancers active during embryonic development but silent in the adult. YAP triggered transcription on promoters by recruiting BRD4, enhancing H3K122 acetylation, and promoting RNApol2 loading and pause-release. YAP also repressed HNF4a target genes by binding to their promoters and enhancers, thus preventing RNApol2 pause-release. YAP activation led to the induction of hepatocyte proliferation, accompanied by tissue remodeling, characterized by polarized macrophages, exhausted T-lymphocytes and dedifferentiation of endothelial cells into proliferative progenitors. Overall, these analyses suggest that YAP is a master regulator of liver function that reshapes the enhancer landscape to control transcription of genes involved in metabolism, proliferation, and inflammation, subverts lineage specification programs by antagonizing HNF4a and modulating the immune infiltrate and the vascular architecture of the liver.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.