ArticleGenes & cancer2010
Transcriptional and Translational Downregulation of Thioredoxin Interacting Protein Is Required for Metabolic Reprogramming during G(1).
Article in Genes & cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 72 citations in OpenAlex.
- Harnessing tumor acidity: innovative lactic acid-responsive promoter enables precision control of CAR-T cell activity in solid tumors.Journal for immunotherapy of cancer · 2026Article
- The transcription factor ChREBP Orchestrates liver carcinogenesis by coordinating the PI3K/AKT signaling and cancer metabolism.Nature communications · 2024Article
- The role of TXNIP in cancer: a fine balance between redox, metabolic, and immunological tumor control.British journal of cancer · 2023Review
- The stress-responsive protein REDD1 and its pathophysiological functions.Experimental & molecular medicine · 2023Review
- CTLA4 protects against maladaptive cytotoxicity during the differentiation of effector and follicular CD4Cellular & molecular immunology · 2023Article
- BCR-ABL triggers a glucose-dependent survival program during leukemogenesis through the suppression of TXNIP.Cell death & disease · 2023Article
- MEK1-dependent MondoA phosphorylation regulates glucose uptake in response to ketone bodies in colorectal cancer cells.Cancer science · 2023Article
- TXNIP loss expands Myc-dependent transcriptional programs by increasing Myc genomic binding.PLoS biology · 2023Article
- Insulin-like growth factors and aging: lessons from Laron syndrome.Frontiers in endocrinology · 2023Review
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- The HDAC Inhibitor Butyrate Impairs β Cell Function and Activates the Disallowed Gene Hexokinase I.International journal of molecular sciences · 2021Article
- Multiomic characterization of oncogenic signaling mediated by wild-type and mutant RIT1.Science signaling · 2021Article
- TSHZ2 is an EGF-regulated tumor suppressor that binds to the cytokinesis regulator PRC1 and inhibits metastasis.Science signaling · 2021Article
- UHRF1 Induces Methylation of theMolecules and cells · 2021Article
- The Emerging Role of TXNIP in Ischemic and Cardiovascular Diseases; A Novel Marker and Therapeutic Target.International journal of molecular sciences · 2021Review
- Protein synthesis inhibitors stimulate MondoA transcriptional activity by driving an accumulation of glucose 6-phosphate.Cancer & metabolism · 2020Article
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Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Growth factor signaling drives increased glucose uptake and glycolysis-the Warburg effect-that supports macromolecular synthesis necessary for cell growth and proliferation. Thioredoxin interacting protein (TXNIP), a direct and glucose-induced transcriptional target of MondoA, is a potent negative regulator of glucose uptake and utilization. Thus, TXNIP may inhibit cell growth by restricting substrate availability for macromolecular synthesis. To determine TXNIP's contribution to metabolic reprogramming, we examined MondoA and TXNIP as cells exit quiescence and enter G(1). Serum stimulation of quiescent immortal diploid fibroblasts resulted in an acute upregulation of glucose uptake and glycolysis coinciding with downregulation of TXNIP expression. Ectopic expression of either MondoA or TXNIP restricted cell growth by blocking glucose uptake. Mechanistically, Ras-MAPK and PI3K/Akt signaling inhibit TXNIP translation and MondoA-dependent TXNIP transcription, respectively. We propose that the coordinated downregulation of MondoA transcriptional activity at the TXNIP promoter and inhibition of TXNIP translation are key components of metabolic reprogramming required for cells to exit quiescence.
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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.