ArticleThe Biochemical journal2013
MondoA senses adenine nucleotides: transcriptional induction of thioredoxin-interacting protein.
Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- 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
- Regulation of Normal and Neoplastic Proliferation and Metabolism by the Extended Myc Network.Cells · 2022Review
- Review
- The Role of Mondo Family Transcription Factors in Nutrient-Sensing and Obesity.Frontiers in endocrinology · 2021Review
- 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
- Beyond the Warburg Effect: N-Myc Contributes to Metabolic Reprogramming in Cancer Cells.Frontiers in oncology · 2020Review
- Cellular acidosis triggers human MondoA transcriptional activity by driving mitochondrial ATP production.eLife · 2019Article
- 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
- New Insight Into Metformin Action: Regulation of ChREBP and FOXO1 Activities in Endothelial Cells.Molecular endocrinology (Baltimore, Md.) · 2015Article
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- Deregulated Myc requires MondoA/Mlx for metabolic reprogramming and tumorigenesis.Cancer cell · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The MondoA-Mlx transcription complex plays a pivotal role in glucose homoeostasis by activating target gene expression in response to G6P (glucose 6-phosphate), the first reaction intermediate in glycolysis. TXNIP (thioredoxin-interacting protein) is a direct and glucose-responsive target of MondoA that triggers a negative-feedback loop by restricting glucose uptake when G6P levels increase. We show in the present study that TXNIP expression is also activated by AICAR (5-amino-4-imidazolecarboxamide ribofuranoside) and adenosine. Using pharmacological inhibitors and genetic knockdowns of purine metabolic enzymes, we establish that TXNIP induction by AICAR and adenosine requires their cellular uptake and metabolism to adenine nucleotides. AICAR induction of TXNIP depended on MondoA, but was independent of AMPK (AMP-activated protein kinase) activation and calcium. The findings of the present study have two important implications. First, in addition to activating AMPK, AICAR may have AMPK-independent effects on gene expression by regulating MondoA-Mlx activity following its flux into the adenine nucleotide pool. Secondly, MondoA-Mlx complexes sense elevated levels of G6P and adenine nucleotides to trigger a TXNIP-dependent feedback inhibition of glycolysis. We propose that this mechanism serves as a checkpoint to restore metabolic homoeostasis.
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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.