ArticleMolecular and cellular biology2015
MondoA-Mlx transcriptional activity is limited by mTOR-MondoA interaction.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Autophagy in kidney physiology: from cellular quality control to organ metabolism.Autophagy reports · 2026Review
- MondoA and AKI and AKI-to-CKD Transition.Journal of the American Society of Nephrology : JASN · 2024Article
- The transcription factor ChREBP Orchestrates liver carcinogenesis by coordinating the PI3K/AKT signaling and cancer metabolism.Nature communications · 2024Article
- Sulforaphane acutely activates multiple starvation response pathways.Frontiers in nutrition · 2024Article
- The Function of MondoA and ChREBP Nutrient-Sensing Factors in Metabolic Disease.International journal of molecular sciences · 2023Review
- TXNIP loss expands Myc-dependent transcriptional programs by increasing Myc genomic binding.PLoS biology · 2023Article
- Immunomodulatory Role of Thioredoxin Interacting Protein in Cancer's Impediments: Current Understanding and Therapeutic Implications.Vaccines · 2022Review
- Article
- 3-Bromopyruvic acid regulates glucose metabolism by targeting the c-Myc/TXNIP axis and induces mitochondria-mediated apoptosis in TNBC cells.Experimental and therapeutic medicine · 2022Article
- Review
- The Role of Mondo Family Transcription Factors in Nutrient-Sensing and Obesity.Frontiers in endocrinology · 2021Review
- Protein synthesis inhibitors stimulate MondoA transcriptional activity by driving an accumulation of glucose 6-phosphate.Cancer & metabolism · 2020Article
- MondoA:MLX complex regulates glucose-dependent gene expression and links to circadian rhythm in liver and brain of the freeze-tolerant wood frog, Rana sylvatica.Molecular and cellular biochemistry · 2020Article
- TXNIP/TBP-2: A Master Regulator for Glucose Homeostasis.Antioxidants (Basel, Switzerland) · 2020Review
- TXNIP mediates high glucose-induced mitophagic flux and lysosome enlargement in human retinal pigment epithelial cells.Biology open · 2019Article
- Cellular acidosis triggers human MondoA transcriptional activity by driving mitochondrial ATP production.eLife · 2019Article
- Ras Suppresses TXNIP Expression by Restricting Ribosome Translocation.Molecular and cellular biology · 2018Article
- Single-Nucleotide Polymorphism of the MLX Gene Is Associated With Takayasu Arteritis.Circulation. Genomic and precision medicine · 2018Article
- The manifold role of the mitochondria in skeletal muscle insulin resistance.Current opinion in clinical nutrition and metabolic care · 2018Review
- Expression of TXNIP in Cancer Cells and Regulation by 1,25(OH)₂D₃: Is It Really the Vitamin D₃ Upregulated Protein?International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mammalian target of rapamycin (mTOR) integrates multiple signals, including nutrient status, growth factor availability, and stress, to regulate cellular and organismal growth. How mTOR regulates transcriptional programs in response to these diverse stimuli is poorly understood. MondoA and its obligate transcription partner Mlx are basic helix-loop-helix leucine zipper (bHLHZip) transcription factors that sense and execute a glucose-responsive transcriptional program. MondoA-Mlx complexes activate expression of thioredoxin-interacting protein (TXNIP), which is a potent inhibitor of cellular glucose uptake and aerobic glycolysis. Both mTOR and MondoA are central regulators of glucose metabolism, yet whether they interact physically or functionally is unknown. We show that inhibition of mTOR induces MondoA-dependent expression of TXNIP, coinciding with reduced glucose uptake. Mechanistically, mTOR binds to MondoA in the cytoplasm and prevents MondoA-Mlx complex formation, restricting MondoA's nuclear entry and reducing TXNIP expression. Further, we show that mTOR inhibitors and reactive oxygen species (ROS) regulate interaction between MondoA and mTOR in an opposing manner. Like mTOR's suppression of the MondoA-TXNIP axis, MondoA can also suppress mTOR complex 1 (mTORC1) activity via its direct transcriptional regulation of TXNIP. Collectively, these studies reveal a regulatory relationship between mTOR and the MondoA-TXNIP axis that we propose contributes to glucose homeostasis.
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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.