ArticleMolecular endocrinology (Baltimore, Md.)2009
Adenosine-containing molecules amplify glucose signaling and enhance txnip expression.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- The Function of MondoA and ChREBP Nutrient-Sensing Factors in Metabolic Disease.International journal of molecular sciences · 2023Review
- Review
- The Role of Mondo Family Transcription Factors in Nutrient-Sensing and Obesity.Frontiers in endocrinology · 2021Review
- Thioredoxin-Interacting Protein (TXNIP) with Focus on Brain and Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Expression of recombinant classical swine fever virus E2 glycoprotein by endogenous Txnip promoter in stable transgenic CHO cells.Engineering in life sciences · 2020Article
- Glucose-6-Phosphate Upregulates Txnip Expression by Interacting With MondoA.Frontiers in molecular biosciences · 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
- The Function of Thioredoxin-Binding Protein-2 (TBP-2) in Different Diseases.Oxidative medicine and cellular longevity · 2018Review
- Investigation of the influence of high glucose on molecular and genetic responses: anGenes & nutrition · 2018Article
- Phosphorylation of TXNIP by AKT Mediates Acute Influx of Glucose in Response to Insulin.Cell reports · 2017Article
- The glucose-sensing transcription factor MLX promotes myogenesis via myokine signaling.Genes & development · 2015Article
- New Insight Into Metformin Action: Regulation of ChREBP and FOXO1 Activities in Endothelial Cells.Molecular endocrinology (Baltimore, Md.) · 2015Article
- The synergism of MCL1 and glycolysis on pediatric acute lymphoblastic leukemia cell survival and prednisolone resistance.Haematologica · 2013Article
- Thioredoxin Interacting Protein (TXNIP) and Pathogenesis of Diabetic Retinopathy.Journal of clinical & experimental ophthalmology · 2013Article
- MondoA senses adenine nucleotides: transcriptional induction of thioredoxin-interacting protein.The Biochemical journal · 2013Article
- Thioredoxin and thioredoxin target proteins: from molecular mechanisms to functional significance.Antioxidants & redox signaling · 2013Review
- AMPK-dependent degradation of TXNIP upon energy stress leads to enhanced glucose uptake via GLUT1.Molecular cell · 2013Article
- Glucose induces protein targeting to glycogen in hepatocytes by fructose 2,6-bisphosphate-mediated recruitment of MondoA to the promoter.Molecular and cellular biology · 2013Article
- Article
- Redox regulation by nuclear factor erythroid 2-related factor 2: gatekeeping for the basal and diabetes-induced expression of thioredoxin-interacting protein.Molecular pharmacology · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eukaryotic cells sense extracellular glucose concentrations via diverse mechanisms to regulate the expression of genes involved in metabolic control. One such example is the tight correlation between the expression of thioredoxin-interacting protein (Txnip) and extracellular glucose levels. In this report, we show that the transcription of the Txnip gene is induced by adenosine-containing molecules, of which an intact adenosine moiety is necessary and sufficient. Txnip promoter contains a carbohydrate response element, which mediates the induction of Txnip expression by these molecules in a glucose-dependent manner. Max-like protein X and MondoA are transcription factors previously shown to stimulate glucose-dependent Txnip expression and are shown here to convey stimulatory signals from extracellular adenosine-containing molecules to the Txnip promoter. The regulatory role of these molecules may be exerted via amplifying glucose signaling. Hence, this revelation may pave the way for interventions aimed toward metabolic disorders resulting from abnormal 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.