ArticleScientific reports2017
RNA helicase DDX3 maintains lipid homeostasis through upregulation of the microsomal triglyceride transfer protein by interacting with HNF4 and SHP.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- DDX3X overexpression in mice can cause rapid tissue-specific toxicity and mortality.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Liquid-liquid phase separation-driven regulated cell death: from molecular mechanisms to therapeutic strategies.Cell death discovery · 2026Review
- A genetic interaction between DED1 and HAT1 in Saccharomyces cerevisiae reveals a role for Hat1p in cytoplasmic RNA granule accumulation.G3 (Bethesda, Md.) · 2026Article
- Hepatocyte nuclear factors dynamically regulate triglyceride metabolic reprogramming in metabolic dysfunction-associated steatotic liver disease: Mechanisms and implications.World journal of hepatology · 2025Review
- A novel reporter for helicase activity in translation uncovers DDX3X interactions.RNA (New York, N.Y.) · 2024Article
- Integrating text mining with network models for successful target identification:Frontiers in pharmacology · 2024Article
- Non-Vesicular Lipid Transport Machinery inInternational journal of molecular sciences · 2023Review
- Protective and Adverse Roles of DDX3X in Different Cell Types in Nonalcoholic Steatohepatitis Progression.Research (Washington, D.C.) · 2023Article
- Lack of TRPV1 Channel Modulates Mouse Gene Expression and Liver Proteome with Glucose Metabolism Changes.International journal of molecular sciences · 2022Article
- DEAD-box helicase 27 enhances stem cell-like properties with poor prognosis in breast cancer.Journal of translational medicine · 2021Article
- Level of Murine DDX3 RNA Helicase Determines Phenotype Changes of Hepatocytes In Vitro and In Vivo.International journal of molecular sciences · 2021Article
- Targeting host DEAD-box RNA helicase DDX3X for treating viral infections.Antiviral research · 2021Review
- Whole Lotta Lipids-from HCV RNA Replication to the Mature Viral Particle.International journal of molecular sciences · 2020Review
- DEAD-box RNA Helicase DDX3: Functional Properties and Development of DDX3 Inhibitors as Antiviral and Anticancer Drugs.Molecules (Basel, Switzerland) · 2020Review
- Small Molecule Screen Reveals Joint Regulation of Stress Granule Formation and Lipid Droplet Biogenesis.Frontiers in cell and developmental biology · 2020Article
- Divergent organ-specific isogenic metastatic cell lines identified using multi-omics exhibit differential drug sensitivity.PloS one · 2020Article
- p300/CBP as a Key Nutritional Sensor for Hepatic Energy Homeostasis and Liver Fibrosis.BioMed research international · 2018Review
- Non-vesicular Lipid Transport Machinery inFrontiers in cellular and infection microbiology · 2018Review
- DDX3 localizes to the centrosome and prevents multipolar mitosis by epigenetically and translationally modulating p53 expression.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multifunctional RNA helicase DDX3 participates in HCV infection, one of the major causes of hepatic steatosis. Here, we investigated the role of DDX3 in hepatic lipid metabolism. We found that HCV infection severely reduced DDX3 expression. Analysis of intracellular triglyceride and secreted ApoB indicated that lipid accumulations were increased while ApoB secretion were decreased in DDX3 knockdown HuH7 and HepG2 cell lines. Down-regulation of DDX3 significantly decreased protein and transcript expression of microsomal triglyceride transfer protein (MTP), a key regulator of liver lipid homeostasis. Moreover, DDX3 interacted with hepatocyte nuclear factor 4 (HNF4) and small heterodimer partner (SHP), and synergistically up-regulated HNF4-mediated transactivation of MTP promoter via its ATPase activity. Further investigation revealed that DDX3 interacted with CBP/p300 and increased the promoter binding affinity of HNF4 by enhancing HNF4 acetylation. Additionally, DDX3 partially relieved the SHP-mediated suppression on MTP promoter by competing with SHP for HNF4 binding which disrupted the inactive HNF4/SHP heterodimer while promoted the formation of the active HNF4 homodimer. Collectively, these results imply that DDX3 regulates MTP gene expression and lipid homeostasis through interplay with HNF4 and SHP, which may also reveal a novel mechanism of HCV-induced steatosis.
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