ArticleInternational journal of cell biology2013
C-Terminal Binding Protein: A Molecular Link between Metabolic Imbalance and Epigenetic Regulation in Breast Cancer.
Article in International journal of cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- Carvacrol from Moringa oleifera as a potential antidiabetic agent using integrated in-silico approach inhibiting TCF7L2.Scientific reports · 2026Article
- CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells.Molecular carcinogenesis · 2025Article
- The transcriptional repressor Ctbp2 as a metabolite sensor regulating cardiomyocytes proliferation and heart regeneration.Molecular medicine (Cambridge, Mass.) · 2025Article
- Transcriptional corepressor activity of CtBP1 is regulated by ISG15 modification.Animal cells and systems · 2024Article
- JAC4 Inhibits EGFR-Driven Lung Adenocarcinoma Growth and Metastasis through CTBP1-Mediated JWA/AMPK/NEDD4L/EGFR Axis.International journal of molecular sciences · 2023Article
- Exploring the Genetic Predisposition to Epigenetic Changes in Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Transcriptomics and Metabolomics Integration Reveals Redox-Dependent Metabolic Rewiring in Breast Cancer Cells.Cancers · 2021Article
- Article
- CtBP modulates Snail-mediated tumor invasion in Drosophila.Cell death discovery · 2021Article
- Protocatechuic Aldehyde Represses Proliferation and Migration of Breast Cancer Cells through Targeting C-terminal Binding Protein 1.Journal of breast cancer · 2020Article
- C-terminal binding proteins 1 and 2 in traumatic brain injury-induced inflammation and their inhibition as an approach for anti-inflammatory treatment.International journal of biological sciences · 2020Article
- Human iPSC-Derived Neuronal Cells FromFrontiers in neuroscience · 2020Article
- Disruption of redox homeostasis for combinatorial drug efficacy inCancer & metabolism · 2020Article
- Epigenetic re-wiring of breast cancer by pharmacological targeting of C-terminal binding protein.Cell death & disease · 2019Article
- A pathogenic CtBP1 missense mutation causes altered cofactor binding and transcriptional activity.Neurogenetics · 2019Article
- Mechanisms contributing to persistently activated cell phenotypes in pulmonary hypertension.The Journal of physiology · 2019Review
- C-Terminal Binding Protein 1 Modulates Cellular Redox via Feedback Regulation of MPC1 and MPC2 in Melanoma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- CPP-E1A fusion peptides inhibit CtBP-mediated transcriptional repression.Molecular oncology · 2018Article
- Hallmarks of Pulmonary Hypertension: Mesenchymal and Inflammatory Cell Metabolic Reprogramming.Antioxidants & redox signaling · 2018Review
- The intracellular NADH level regulates atrophic nonunion pathogenesis through the CtBP2-p300-Runx2 transcriptional complex.International journal of biological sciences · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The prevalence of obesity has given rise to significant global concerns as numerous population-based studies demonstrate an incontrovertible association between obesity and breast cancer. Mechanisms proposed to account for this linkage include exaggerated levels of carbohydrate substrates, elevated levels of circulating mitogenic hormones, and inflammatory cytokines that impinge on epithelial programming in many tissues. Moreover, recently many scientists have rediscovered the observation, first described by Otto Warburg nearly a century ago, that most cancer cells undergo a dramatic metabolic shift in energy utilization and expenditure that fuels and supports the cellular expansion associated with malignant proliferation. This shift in substrate oxidation comes at the cost of sharp changes in the levels of the high energy intermediate, nicotinamide adenine dinucleotide (NADH). In this review, we discuss a novel example of how shifts in the concentration and flux of substrates metabolized and generated during carbohydrate metabolism represent components of a signaling network that can influence epigenetic regulatory events in the nucleus. We refer to this regulatory process as "metabolic transduction" and describe how the C-terminal binding protein (CtBP) family of NADH-dependent nuclear regulators represents a primary example of how cellular metabolic status can influence epigenetic control of cellular function and fate.
Identifiers
What OpenQuestion holds
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.