Evidence map›Paper›PMID 20080798›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Regulation of NF-kappaB by NSD1/FBXL11-dependent reversible lysine methylation of p65.

Tao Lu, Mark W Jackson, Benlian Wang, Maojing Yang, Mark R Chance, Masaru Miyagi, Andrei V Gudkov, George R Stark

Open access · greenAbstract read
In one paragraph

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 185 papers.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed
5.8field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

185 citing papers in PubMed, 280 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Many faces of mammalian NSD methyltransferases.Cellular & molecular biology letters · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Histone demethylases in autophagy and inflammation.Cell communication and signaling : CCS · 2025
    Review
  17. Discovery and structural studies of histone demethylases.Frontiers in epigenetics and epigenomics · 2025
    Review
  18. Lysine and arginine methylation of transcription factors.Cellular and molecular life sciences : CMLS · 2024
    Review
  19. Review
  20. Article

125 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Tao LuDepartment of Molecular Genetics, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Mark W Jackson
Benlian Wang
Maojing Yang
Mark R Chance
Masaru Miyagi
Andrei V Gudkov
George R Stark
Case Western Reserve University · USCase Comprehensive Cancer CenterCleveland Clinic · USRoswell Park Comprehensive Cancer Center · US

Funding

Negative Regulators of NFkappaBR01CA095851 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI STARK, GEORGE ROBERT · 2003 to 2012
$2.7M
GENETIC ELEMENTS TRANSFORMING MOUSE FIBROBLASTSR01CA060730 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GUDKOV, ANDREI V · 1994 to 2009
$2.6M
NCI NIH HHS CA60730NCI NIH HHS CA95851NCI NIH HHS R01 CA060730NCI NIH HHS R01 CA095851
6 · The paper itself

Abstract

NF-kappaB, a central coordinator of immune and inflammatory responses, must be tightly regulated. We describe a NF-kappaB regulatory pathway that is driven by reversible lysine methylation of the p65 subunit, carried out by a lysine methylase, the nuclear receptor-binding SET domain-containing protein 1 (NSD1), and a lysine demethylase, F-box and leucine-rich repeat protein 11 (FBXL11). Overexpression of FBXL11 inhibits NF-kappaB activity, and a high level of NSD1 activates NF-kappaB and reverses the inhibitory effect of FBXL11, whereas reduced expression of NSD1 decreases NF-kappaB activation. The targets are K218 and K221 of p65, which are methylated in cells with activated NF-kappaB. Overexpression of FBXL11 slowed the growth of HT29 cancer cells, whereas shRNA-mediated knockdown had the opposite effect, and these phenotypes were dependent on K218/K221 methylation. In mouse embryo fibroblasts, the activation of most p65-dependent genes relied on K218/K221 methylation. Importantly, expression of the FBXL11 gene is driven by NF-kappaB, revealing a negative regulatory feedback loop. We conclude that reversible lysine methylation of NF-kappaB is an important element in the complex regulation of this key transcription factor.

Indexed as

Amino Acid SequenceAnimalsCell Line, TumorCell ProliferationCells, CulturedCytokinesEmbryo, MammalianF-Box ProteinsFibroblastsGene Expression RegulationHistone DemethylasesHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHumansIntracellular Signaling Peptides and ProteinsJumonji Domain-Containing Histone DemethylasesCytokinesF-Box ProteinsFBXL11 protein, mouseHistone DemethylasesHistone-Lysine N-MethyltransferaseHistone MethyltransferasesIntracellular Signaling Peptides and ProteinsJumonji Domain-Containing Histone DemethylasesKDM2A protein, humanLysineNSD1 protein, humanNuclear ProteinsOxidoreductases, N-DemethylatingProtein MethyltransferasesProtein SubunitsTranscription Factor RelA

Identifiers

PMID20080798
PMCPMC2806709
OpenAlexW2111098183

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.