ArticleMolecular biology reports2012
Negative transcriptional regulation of inflammatory genes by group B3 vitamin nicotinamide.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 13 citations in OpenAlex.
- Recent Advances on the Role of B Vitamins in Cancer Prevention and Progression.International journal of molecular sciences · 2025Review
- The impact of aging and oxidative stress in metabolic and nervous system disorders: programmed cell death and molecular signal transduction crosstalk.Frontiers in immunology · 2023Review
- Innovative therapeutic strategies for cardiovascular disease.EXCLI journal · 2023Review
- Nicotinamide as a Foundation for Treating Neurodegenerative Disease and Metabolic Disorders.Current neurovascular research · 2021Review
- Article
- Nicotinamide: Oversight of Metabolic Dysfunction Through SIRT1, mTOR, and Clock Genes.Current neurovascular research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The water-soluble group B3 vitamin nicotinamide (NAM) is involved in a wide range of physical processes through biosynthetically converted to nicotinamide adenine dinucleotide (NAD(+)). In addition to its pivotal role in energy metabolism, NAD(+) is also the indispensable substrate of poly (ADP-ribose) polymerase-1 (PARP-1) and sirtuin 1 (SIRT1). PARP-1 and SIRT1 may catalyze the posttranslational poly(ADP-ribosyl)ation and acetylation of histones as well as non-histone proteins, such as nuclear factor kappa B and activator protein 1, which play crucial roles in transcriptional regulation of inflammatory genes. The NAD(+)-dependent modifications catalyzed by PARP-1 and SIRT1 liberate NAM, and NAM acts as feedback inhibitor of PARP-1 and SIRT1 through interacting with the enzymes at the binding site for NAD(+). There is increasing evidence that NAM effectively suppresses the expression of inflammatory genes and provides therapeutic benefits in various inflammation-based diseases. The mechanisms underlie the anti-inflammatory properties of NAM might involve the inhibition of PARP-1 and SIRT1.
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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.