ArticleGenes & development2016
The LATS2 tumor suppressor inhibits SREBP and suppresses hepatic cholesterol accumulation.
Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed.
- VGLL4 enhances PDK4 transcription and promotes metabolic dysfunction-associated fatty liver disease.EMBO reports · 2026Article
- Temporal transcriptomic changes during neurodevelopment in a mouse model of Smith-Lemli-Opitz syndrome.The Journal of steroid biochemistry and molecular biology · 2026Article
- A YAP/TAZ-CDC6 Axis Initiates and Maintains Malignant Transformation.Cancer science · 2026Article
- Genome-wide CRISPR/Cas9 screening reveals lipid metabolism and inflammatory signalling as modulators of ganoderic acid DM cytotoxicity.Journal of genetics · 2026Article
- Cholesterol Overload Drives Hepatic Steatosis by Inhibiting OGT-dependent PPARα O-GlcNAcylation and Transactivation.International journal of biological sciences · 2026Article
- CircRNA_01754 Regulates Milk Fat Production Through the Hippo Signaling Pathway.Animals : an open access journal from MDPI · 2025Article
- Cholesterol metabolism on stem cell fate determination: a frontier horizon.Stem cell research & therapy · 2025Review
- Temporal transcriptomic changes during neurodevelopment in a mouse model of Smith-Lemli-Opitz syndrome.bioRxiv : the preprint server for biology · 2025Article
- Intestinal alkaline phosphatase is a receptor for cholesterol-lowering pentapeptide IIAEK and regulates cholesterol homeostasis in mice.Scientific reports · 2025Article
- Phosphorylation of an RNA-Binding Protein Rck/Me31b by Hippo Is Essential for Adipose Tissue Aging.Aging cell · 2025Article
- Unlocking the lipid code: SREBPs as key drivers in gastrointestinal tumour metabolism.Lipids in health and disease · 2025Review
- Hippo-YAP/TAZ-ROS signaling axis regulates metaflammation induced by SelenoM deficiency in high-fat diet-derived obesity.Journal of advanced research · 2025Article
- Mammalian Ste20-like kinase 1 regulates AMPK to mitigate the progression of non-alcoholic fatty liver disease.European journal of medical research · 2025Article
- Review
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Genomic and transcriptomic analyses of Heteropoda venatoria reveal the expansion of P450 family for starvation resistance in spiders.GigaScience · 2025Article
- Regulation of Hippo-YAP1/TAZ pathway in metabolic dysfunction-associated steatotic liver disease.Frontiers in pharmacology · 2025Review
- SREBP2 as a central player in cancer progression: potential for targeted therapeutics.Frontiers in pharmacology · 2025Review
- Article
- Interplay between YAP/TAZ and metabolic dysfunction-associated steatotic liver disease progression.Archives of pharmacal research · 2024Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
The Hippo signaling pathway is a major regulator of organ size. In the liver, Hippo pathway deregulation promotes hyperplasia and hepatocellular carcinoma primarily through hyperactivation of its downstream effector, YAP. The LATS2 tumor suppressor is a core member of the Hippo pathway. A screen for LATS2-interacting proteins in liver-derived cells identified the transcription factor SREBP2, master regulator of cholesterol homeostasis. LATS2 down-regulation caused SREBP activation and accumulation of excessive cholesterol. Likewise, mice harboring liver-specific Lats2 conditional knockout (Lats2-CKO) displayed constitutive SREBP activation and overexpressed SREBP target genes and developed spontaneous fatty liver disease. Interestingly, the impact of LATS2 depletion on SREBP-mediated transcription was clearly distinct from that of YAP overexpression. When challenged with excess dietary cholesterol, Lats2-CKO mice manifested more severe liver damage than wild-type mice. Surprisingly, apoptosis, inflammation, and fibrosis were actually attenuated relative to wild-type mice, in association with impaired p53 activation. Subsequently, Lats2-CKO mice failed to recover effectively from cholesterol-induced damage upon return to a normal diet. Additionally, decreased LATS2 mRNA in association with increased SREBP target gene expression was observed in a subset of human nonalcoholic fatty liver disease cases. Together, these findings further highlight the tight links between tumor suppressors and metabolic homeostasis.
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