ArticleCellular and molecular gastroenterology and hepatology2022
Coordinated Cross-Talk Between the Myc and Mlx Networks in Liver Regeneration and Neoplasia.
Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- MYC Binding Near Transcriptional End Sites Regulates Basal Gene Expression, Read-Through Transcription, and Intragenic Contacts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Gas1-Mediated Suppression of Hepatoblastoma Tumorigenesis.The American journal of pathology · 2025Article
- Muscle fiber Myc is dispensable for muscle growth and its forced expression severely perturbs homeostasis.Nature communications · 2025Article
- MLX phosphorylation stabilizes the ChREBP-MLX heterotetramer on tandem E-boxes to control carbohydrate and lipid metabolism.Science advances · 2025Article
- MLX phosphorylation stabilizes the ChREBP-MLX heterotetramer on tandem E-boxes to control carbohydrate and lipid metabolism.bioRxiv : the preprint server for biology · 2024Article
- Body-Wide Inactivation of the Myc-Like Mlx Transcription Factor Network Accelerates Aging and Increases the Lifetime Cancer Incidence.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Manipulating Myc for reparative regeneration.Frontiers in cell and developmental biology · 2024Review
- Multi-omics reveals goose fatty liver formation from metabolic reprogramming.Frontiers in veterinary science · 2024Article
- Endothelial c-Myc knockout disrupts metabolic homeostasis and triggers the development of obesity.Frontiers in cell and developmental biology · 2024Article
- The Myc-Like Mlx Network Impacts Aging and Metabolism.bioRxiv : the preprint server for biology · 2023Article
- Premature aging and reduced cancer incidence associated with near-complete body-wide Myc inactivation.Cell reports · 2023Article
- Myc beyond Cancer: Regulation of Mammalian Tissue Regeneration.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- Lessons in aging from Myc knockout mouse models.Frontiers in cell and developmental biology · 2023Review
- Disruption of Multiple Overlapping Functions Following Stepwise Inactivation of the Extended Myc Network.Cells · 2022Article
- Regulation of Normal and Neoplastic Proliferation and Metabolism by the Extended Myc Network.Cells · 2022Review
- Review
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsThe c-Myc (Myc) Basic helix-loop-helix leucine zipper (bHLH-ZIP) transcription factor is deregulated in most cancers. In association with Max, Myc controls target genes that supervise metabolism, ribosome biogenesis, translation, and proliferation. This Myc network crosstalks with the Mlx network, which consists of the Myc-like proteins MondoA and ChREBP, and Max-like Mlx. Together, this extended Myc network regulates both common and distinct gene targets. Here, we studied the consequence of Myc and/or Mlx ablation in the liver, particularly those pertaining to hepatocyte proliferation, metabolism, and spontaneous tumorigenesis.
methodsWe examined the ability of hepatocytes lacking Mlx (MlxKO) or Myc+Mlx (double KO [DKO]) to repopulate the liver over an extended period of time in a murine model of type I tyrosinemia. We also compared this and other relevant behaviors, phenotypes, and transcriptomes of the livers with those from previously characterized MycKO, ChrebpKO, and MycKO × ChrebpKO mice.
resultsHepatocyte regenerative potential deteriorated as the Extended Myc Network was progressively dismantled. Genes and pathways dysregulated in MlxKO and DKO hepatocytes included those pertaining to translation, mitochondrial function, and hepatic steatosis resembling nonalcoholic fatty liver disease. The Myc and Mlx Networks were shown to crosstalk, with the latter playing a disproportionate role in target gene regulation. All cohorts also developed steatosis and molecular evidence of early steatohepatitis. Finally, MlxKO and DKO mice showed extensive hepatic adenomatosis.
conclusionsIn addition to showing cooperation between the Myc and Mlx Networks, this study showed the latter to be more important in maintaining proliferative, metabolic, and translational homeostasis, while concurrently serving as a suppressor of benign tumorigenesis. GEO accession numbers: GSE181371, GSE130178, and GSE114634.
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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.