ReviewCancer research2015
NF-κB: Regulation by Methylation.
Review in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
65 citing papers in PubMed, 100 citations in OpenAlex.
- Celebrating the 40-year milestone: NF-ĸB in oncoimmunity.Cancer letters · 2026Review
- Claudin and Rab proteins are key molecular components involved in coccidiosis resistance in Portuguese Merino sheep.Genetics, selection, evolution : GSE · 2025Article
- DNA methyltransferase 1 correlates with immune modulation in pancreatic neuroendocrine tumors.Scientific reports · 2025Article
- DNA hypomethylated modified lncRNA MALAT1 promotes atherosclerotic cardiovascular disease progression through NF-κB signaling pathway regulating cholesterol metabolism and inflammatory response.Biochemistry and biophysics reports · 2025Article
- Decoding NF-κB: nucleocytoplasmic shuttling dynamics, synthetic modulation and post-therapeutic behavior in cancer.Molecular biology reports · 2025Review
- A new type of Caspase-1 upon recognizing bacteria inhibits GSDME-dependent histone modification and NF-κB signaling.Communications biology · 2025Article
- USP39 promote post-translational modifiers to stimulate the progress of cancer.Discover oncology · 2025Review
- Mutational Landscape of Bone Marrow CD19 and CD138 Cells in Waldenström Macroglobulinemia (WM) and IgM Monoclonal Gammopathy of Undetermined Significance (IgM MGUS).Cancer medicine · 2024Article
- Programmed cell death-ligand 2: new insights in cancer.Frontiers in immunology · 2024Review
- Genetic Alterations of NF-κB and Its Regulators: A Rich Platform to Advance Colorectal Cancer Diagnosis and Treatment.International journal of molecular sciences · 2023Review
- KDM2A Deficiency in the Liver Promotes Abnormal Liver Function and Potential Liver Damage.Biomolecules · 2023Article
- JMJD6 protects against isoproterenol-induced cardiac hypertrophy via inhibition of NF-κB activation by demethylating R149 of the p65 subunit.Acta pharmacologica Sinica · 2023Article
- New Insights into NF-κB Signaling in Innate Immunity: Focus on Immunometabolic Crosstalks.Biology · 2023Review
- TNFα Effects on Adipocytes Are Influenced by the Presence of Lysine Methyltransferases, G9a (EHMT2) and GLP (EHMT1).Biology · 2023Article
- Chemopreventive Activity of Ellagitannins fromPlants (Basel, Switzerland) · 2023Article
- (International journal of molecular sciences · 2023Article
- PRMT5 is a therapeutic target in choroidal neovascularization.Scientific reports · 2023Article
- Article
- Proteome-wide identification of non-histone lysine methylation in tomato during fruit ripening.Journal of advanced research · 2022Article
- Endometrial stromal PRMT5 plays a crucial role in decidualization by regulating NF-κB signaling in endometriosis.Cell death discovery · 2022Article
5 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 1 country.
Funding
Abstract
In normal cells exposed to stress, the central transcription factor NF-κB is activated only transiently, to modulate the activation of downstream immune responses. However, in most cancers, NF-κB is abnormally activated constitutively, contributing thus to oncogenesis and tumor progression. Therefore, downregulating NF-κB activity is an important goal of cancer treatment. In order to control NF-κB activity therapeutically, it is helpful to understand the molecular mechanisms that normally govern its activation and how dysregulated NF-κB activity may aid the development of disease. Recent evidence from our laboratories and others indicates that, in addition to various posttranslational modifications of NF-κB that have been observed previously, including phosphorylation, ubiquitination, and acetylation, NF-κB can be methylated reversibly on lysine or arginine residues by histone-modifying enzymes, including lysine and arginine methyl transferases and demethylases. Furthermore, these methylations are required to activate many downstream genes. Interestingly, amplifications and mutations of several such enzymes have been linked to cancer. We propose that some of these mutations may alter the methylation not only of histones but also of NF-κB, making them attractive therapeutic targets.
Indexed as
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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.