ReviewCold Spring Harbor perspectives in medicine2013
Coordination of nutrient availability and utilization by MAX- and MLX-centered transcription networks.
Review in Cold Spring Harbor perspectives in medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed.
- Global profiling of protein lactylation in pancreatic ductal adenocarcinoma.Scientific reports · 2026Article
- Immune evasion: An imperative and consequence of MYC deregulation.Molecular oncology · 2024Review
- The transcription factor ChREBP Orchestrates liver carcinogenesis by coordinating the PI3K/AKT signaling and cancer metabolism.Nature communications · 2024Article
- Glucose-induced and ChREBP: MLX-mediated lipogenic program promotes hepatocellular carcinoma development.Oncogene · 2023Article
- TXNIP loss expands Myc-dependent transcriptional programs by increasing Myc genomic binding.PLoS biology · 2023Article
- Regulation of Normal and Neoplastic Proliferation and Metabolism by the Extended Myc Network.Cells · 2022Review
- 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
- Thioredoxin-Interacting Protein in Cancer and Diabetes.Antioxidants & redox signaling · 2022Review
- Review
- Protein synthesis inhibitors stimulate MondoA transcriptional activity by driving an accumulation of glucose 6-phosphate.Cancer & metabolism · 2020Article
- Differential Fuel Requirements of Human NK Cells and Human CD8 T Cells: Glutamine Regulates Glucose Uptake in Strongly Activated CD8 T Cells.ImmunoHorizons · 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
- Therapeutic Inhibition of Myc in Cancer. Structural Bases and Computer-Aided Drug Discovery Approaches.International journal of molecular sciences · 2018Review
- BRCA1 deficiency sensitizes breast cancer cells to bromodomain and extra-terminal domain (BET) inhibition.Oncogene · 2018Article
- Ras Suppresses TXNIP Expression by Restricting Ribosome Translocation.Molecular and cellular biology · 2018Article
- Myc and ChREBP transcription factors cooperatively regulate normal and neoplastic hepatocyte proliferation in mice.The Journal of biological chemistry · 2018Article
- Precision medicine in pediatric oncology.Molecular and cellular pediatrics · 2018Review
- The MYC transcription factor network: balancing metabolism, proliferation and oncogenesis.Frontiers of medicine · 2018Review
- MAX Mutations in Endometrial Cancer: Clinicopathologic Associations and Recurrent MAX p.His28Arg Functional Characterization.Journal of the National Cancer Institute · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Cell growth and division require the biosynthesis of macromolecule components and cofactors (e.g., nucleotides, lipids, amino acids, and nicotinamide adenine dinucleotide phosphate [NADPH]). Normally, macromolecular biosynthesis is under tight regulatory control, yet these anabolic pathways are often dysregulated in cancer. The resulting metabolic reprogramming of cancer cells is thought to support their high rates of growth and division. The mechanisms that underlie the metabolic changes in cancer are at least partially understood, providing a rationale for their targeting with known or novel therapeutics. This review is focused on how cells sense and respond transcriptionally to essential nutrients, including glucose and glutamine, and how MAX- and MLX-centered transcription networks contribute to metabolic homeostasis in normal and neoplastic cells.
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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.