ArticleEMBO reports2009
Phosphorylation of NF-kappaB p65 at Ser468 controls its COMMD1-dependent ubiquitination and target gene-specific proteasomal elimination.
Article in EMBO reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 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.
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Who cites it
100 citing papers in PubMed, 150 citations in OpenAlex.
- Pneumococcus uses COMMD2 to alter host cellular immunity.Nature communications · 2026Article
- Cuproptosis in inflammation and cancer: molecular mechanisms and therapeutic targets.Molecular cancer · 2026Review
- Telomere Length in Metabolic Syndrome: Mechanisms, Epidemiology and Clinical Implications: A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Soluble CSF1R alleviates microgliopathy in a CSF1R-related leukoencephalopathy (CRL) mouse model.Journal of neuroinflammation · 2025Article
- Vitamin D3 augments cytotoxic effect of Itraconazole on chronic myelogenous leukemia cell line: a synergic effect on AMPK/AKT signaling pathway.Molecular biology reports · 2025Article
- The Interplay Between Obesity and Type 2 Diabetes: Common Pathophysiological Mechanisms Contributing to Telomere Shortening.Life (Basel, Switzerland) · 2025Review
- LGR4 is essential for maintaining β-cell homeostasis through suppression of RANK.Molecular metabolism · 2025Article
- The proximity-based protein interactome and regulatory logics of the transcription factor p65 NF-κB/RELA.EMBO reports · 2025Article
- Unveiling the Cuproptosis in Colitis and Colitis-Related Carcinogenesis: A Multifaceted Player and Immune Moderator.Research (Washington, D.C.) · 2025Review
- Chromatin-associated cullin-RING E3 ubiquitin ligases: keeping transcriptionally active NF-κB in check.Frontiers in immunology · 2025Review
- Structural organization of the retriever-CCC endosomal recycling complex.Nature structural & molecular biology · 2024Article
- WSB1/2 target chromatin-bound lysine-methylated RelA for proteasomal degradation and NF-κB termination.Nucleic acids research · 2024Article
- Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024Review
- Structural Organization of the Retriever-CCC Endosomal Recycling Complex.Research square · 2023Article
- Structural Organization of the Retriever-CCC Endosomal Recycling Complex.bioRxiv : the preprint server for biology · 2023Article
- COMMD proteins function and their regulating roles in tumors.Frontiers in oncology · 2023Review
- Early innate immune response triggered by the human respiratory syncytial virus and its regulation by ubiquitination/deubiquitination processes.Journal of biomedical science · 2022Review
- IKKα plays a major role in canonical NF-κB signalling in colorectal cells.The Biochemical journal · 2022Article
- Canonical and Divergent N-Terminal HBx Isoform Proteins Unveiled: Characteristics and Roles during HBV Replication.Biomedicines · 2021Article
- TRIMs: selective recruitment at different steps of the NF-κB pathway-determinant of activation or resolution of inflammation.Cellular and molecular life sciences : CMLS · 2021Review
40 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
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear factor-kappaB (NF-kappaB) transcription factor system is a crucial component that controls several important biological functions, thus raising the need for mechanisms that ensure the correct termination of its activity. Here, we identify a new phosphorylation/ubiquitination switch in the NF-kappaB network that controls the stability of the transactivating p65 subunit. Tumour necrosis factor-induced phosphorylation of p65 at Ser468 allows binding of COMMD1 and cullin 2, components of a multimeric ubiquitin ligase complex mediating p65 ubiquitination. Mutation of p65 at Ser468 largely prevents p65 ubiquitination and proteasomal degradation. Inducible p65 elimination is restricted to a subset of NF-kappaB target genes such as Icam1. Accordingly, chromatin immunoprecipitation experiments reveal the selective recruitment of Ser468-phosphorylated p65 and COMMD1 to the Icam1 promoter. Phosphorylation of p65 at Ser468 leads to ubiquitin/proteasome-dependent removal of chromatin-bound p65, thus contributing to the selective termination of NF-kappaB-dependent gene expression.
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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.