ArticleThe Journal of biological chemistry2013
Site-specific phosphorylation of the p65 protein subunit mediates selective gene expression by differential NF-κB and RNA polymerase II promoter recruitment.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 69 citations in OpenAlex.
- GINS4 Promotes Neonatal Bronchopulmonary Dysplasia via Driving Phosphorylation and Acetylation of p65 NF-κB.Molecular biotechnology · 2026Article
- Dental pulp stem cells maintain epigenetic chromatin architecture remodeling primed by the etiological stimulus of biliary atresia.Stem cell research & therapy · 2026Article
- Evaluation of the Anti-Inflammatory and Antioxidant Properties ofPreventive nutrition and food science · 2026Article
- Blocking CD30 on CD19 CAR T cells augments their functional capacities against B-cell leukemia/lymphoma.Frontiers in immunology · 2026Article
- Article
- PGAM5 Modulates Macrophage Polarization, Aggravating Inflammation in COPD via the NF-κB Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- Inflammation, diabetic foot and related treatments.Frontiers in endocrinology · 2025Review
- Phosphorylation of RelA/p65 Ser536 inhibits the progression and metastasis of hepatocellular carcinoma by mediating cytoplasmic retention of NF-κB p65.Gastroenterology report · 2024Article
- Novel long non-coding RNAs associated with inflammation and macrophage activation in human.Scientific reports · 2023Article
- The positive regulatory loop of TCF4N/p65 promotes glioblastoma tumourigenesis and chemosensitivity.Clinical and translational medicine · 2022Article
- ADAR3 activates NF-κB signaling and promotes glioblastoma cell resistance to temozolomide.Scientific reports · 2022Article
- Article
- Ubiquitination of NF-κB p65 by FBXW2 suppresses breast cancer stemness, tumorigenesis, and paclitaxel resistance.Cell death and differentiation · 2022Article
- Review
- HJC0416 Attenuates Fibrogenesis in Activated Hepatic Stellate Cells via STAT3 and NF-κB Pathways.The Journal of surgical research · 2021Article
- LncRNA HOTAIR regulates glucose transporter Glut1 expression and glucose uptake in macrophages during inflammation.Scientific reports · 2021Article
- SPNS2 Downregulation Induces EMT and Promotes Colorectal Cancer MetastasisFrontiers in oncology · 2021Article
- Non-Thermal Plasma Couples Oxidative Stress to TRAIL Sensitization through DR5 Upregulation.International journal of molecular sciences · 2020Article
- Dissecting the Regulatory Strategies of NF-κB RelA Target Genes in the Inflammatory Response Reveals Differential Transactivation Logics.Cell reports · 2020Article
- Enhancer-mediated enrichment of interacting JMJD3-DDX21 to ENPP2 locus prevents R-loop formation and promotes transcription.Nucleic acids research · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Phosphorylation of NF-κB plays an important role in modulating transcriptional activity of NF-κB independently of inhibitor of κB (IκB) proteins. For the p65 subunit, multiple phosphorylation sites have been mapped in and adjacent to both the N-terminal Rel homology domain and the C-terminal transactivation domain. Their impact on NF-κB-dependent transcription, however, has never been assessed at a broader level. In this study, we evaluate the importance of differential p65 phosphorylation on four serine acceptor sites in the Rel homology domain for the expression of an array of NF-κB-dependent genes in endothelial cells. We find that inhibition of p65 phosphorylation on these serine residues targets NF-κB activity to distinctive gene subsets in a κB enhancer element-specific context. We show that the phosphorylation-dependent alterations in gene and protein expression are reflective of the amount of p65 and phosphorylated RNA polymerase II (p-RNAP II) bound to respective gene promoter regions. Depending on the gene subset, impaired gene expression was either a result of decreased p65 promoter recruitment or of a failure of bound p65 to recruit p-RNAP II. In conclusion, our findings demonstrate that site-specific p65 phosphorylation targets NF-κB activity to particular gene subsets on a global level by influencing p65 and p-RNAP II promoter recruitment.
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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.