ArticleProceedings of the National Academy of Sciences of the United States of America2010
Nicotinamide adenine dinucleotide (NAD)-regulated DNA methylation alters CCCTC-binding factor (CTCF)/cohesin binding and transcription at the BDNF locus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- NADFrontiers in neurology · 2026Pooled it
- A randomized placebo-controlled trial of nicotinamide riboside in older adults with mild cognitive impairment.GeroScience · 2024Trial
- Whole transcriptome analysis in offspring whose fathers were exposed to a developmental insult: a novel avian model.Scientific reports · 2023Article
- A novel intergenic enhancer that regulatesiScience · 2023Article
- Gene expression analysis of antioxidant and DNA methylation on the rat liver after 4-week wood preservative chromated copper arsenate exposure.Journal of toxicologic pathology · 2023Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- Potential Therapeutic Effects of NAMPT-Mediated NAD Biosynthesis in Depression In Vivo.Brain sciences · 2022Article
- Prognostic value of nicotinamide adenine dinucleotide (NADJournal of gastrointestinal oncology · 2022Article
- Psychostimulants influence oxidative stress and redox signatures: the role of DNA methylation.Redox report : communications in free radical research · 2022Review
- Article
- CTCF as a regulator of alternative splicing: new tricks for an old player.Nucleic acids research · 2021Review
- Cohesin Mutations in Cancer: Emerging Therapeutic Targets.International journal of molecular sciences · 2021Review
- Mitochondrial STAT3 regulates antioxidant gene expression through complex I-derived NAD in triple negative breast cancer.Molecular oncology · 2021Article
- CTCF Mediates Replicative Senescence Through POLD1.Frontiers in cell and developmental biology · 2021Article
- Article
- NADSignal transduction and targeted therapy · 2020Review
- New targeted approaches for epigenetic age predictions.BMC biology · 2020Article
- Nicotinamide Administration Improves Remyelination after Stroke.Neural plasticity · 2017Article
- An NAD+-dependent transcriptional program governs self-renewal and radiation resistance in glioblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- P7C3 Attenuates the Scopolamine-Induced Memory Impairments in C57BL/6J Mice.Neurochemical research · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Cellular metabolism alters patterns of gene expression through a variety of mechanisms, including alterations in histone modifications and transcription factor activity. Nicotinamide adenine dinucleotide (NAD)-dependent proteins such as poly(ADP ribose) polymerases (PARPs) and sirtuin deacetylases play important roles in this regulation, thus NAD provides a crucial link between metabolism and these cellular signaling processes. Here, we found that lowering NAD levels in mouse primary cortical neurons led to decreased activity-dependent BDNF expression. The altered BDNF transcription occurred independently of Sirt or Parp activities; instead, low NAD levels promoted increased DNA methylation of the activity-dependent BDNF promoter. Increased methylation at this promoter triggered the dissociation of the insulator protein CTCF as well as the accompanying cohesin from the BDNF locus. The loss of these proteins resulted in histone acetylation and methylation changes at this locus consistent with chromatin compaction and gene silencing. Because BDNF is critical for neuronal function, these results suggest that age- or nutrition-associated declines in NAD levels as well as deficits in cohesin function associated with disease modulate BDNF expression and could contribute to cognitive impairment.
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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.