ArticleOncogene2016
TAK1 regulates hepatic lipid homeostasis through SREBP.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- The interplay between lipid metabolism, cancer progression and anti-cancer immunity.Experimental & molecular medicine · 2026Review
- Advanced multifunctional nano-delivery platform focusing on treating diseases related to lipid metabolism via targeted intervention in various lipid metabolic processes.Military Medical Research · 2025Review
- Unlocking the lipid code: SREBPs as key drivers in gastrointestinal tumour metabolism.Lipids in health and disease · 2025Review
- USP13 ameliorates nonalcoholic fatty liver disease through inhibiting the activation of TAK1.Journal of translational medicine · 2024Article
- Cholesterol modulates type I/II TGF-β receptor complexes and alters the balance between Smad and Akt signaling in hepatocytes.Communications biology · 2024Article
- Article
- Lipid metabolism and cancer.The Journal of experimental medicine · 2021Review
- Omics-Based Identification of Shared and Gender Disparity Routes inFrontiers in genetics · 2021Article
- TAK1: A Molecular Link Between Liver Inflammation, Fibrosis, Steatosis, and Carcinogenesis.Frontiers in cell and developmental biology · 2021Review
- Fatty liver diseases, mechanisms, and potential therapeutic plant medicines.Chinese journal of natural medicines · 2020Review
- Role of the Sterol Regulatory Element Binding Protein Pathway in Tumorigenesis.Frontiers in oncology · 2020Review
- Innate immune regulatory networks in hepatic lipid metabolism.Journal of molecular medicine (Berlin, Germany) · 2019Review
- Oxysterols and Gastrointestinal Cancers Around the Clock.Frontiers in endocrinology · 2019Review
- SREBP-regulated lipid metabolism: convergent physiology - divergent pathophysiology.Nature reviews. Endocrinology · 2017Review
- Article
- Metabolomic and transcriptomic profiling of hepatocellular carcinomas in Hras12V transgenic mice.Cancer medicine · 2017Article
- Noncanonical cell death program independent of caspase activation cascade and necroptotic modules is elicited by loss of TGFβ-activated kinase 1.Scientific reports · 2017Article
- TAK1 determines susceptibility to endoplasmic reticulum stress and leptin resistance in the hypothalamus.Journal of cell science · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Sterol-regulatory element-binding proteins (SREBPs) are key transcription factors regulating cholesterol and fatty acid biosynthesis. SREBP activity is tightly regulated to maintain lipid homeostasis, and is modulated upon extracellular stimuli such as growth factors. While the homeostatic SREBP regulation is well studied, stimuli-dependent regulatory mechanisms are still elusive. Here we demonstrate that SREBPs are regulated by a previously uncharacterized mechanism through transforming growth factor-β activated kinase 1 (TAK1), a signaling molecule of inflammation. We found that TAK1 binds to and inhibits mature forms of SREBPs. In an in vivo setting, hepatocyte-specific Tak1 deletion upregulates liver lipid deposition and lipogenic enzymes in the mouse model. Furthermore, hepatic Tak1 deficiency causes steatosis pathologies including elevated blood triglyceride and cholesterol levels, which are established risk factors for the development of hepatocellular carcinoma (HCC) and are indeed correlated with Tak1-deficiency-induced HCC development. Pharmacological inhibition of SREBPs alleviated the steatosis and reduced the expression level of the HCC marker gene in the Tak1-deficient liver. Thus, TAK1 regulation of SREBP critically contributes to the maintenance of liver homeostasis to prevent steatosis, which is a potentially important mechanism to prevent HCC development.
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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.