ArticleOncogene2013
GSK3-SCF(FBXW7) targets JunB for degradation in G2 to preserve chromatid cohesion before anaphase.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- Phosphoproteomic and kinase networks reveal partial EMT and stress-adaptive growth programs in pediatric Peutz-Jeghers polyps.Pediatric research · 2026Article
- Oncogenic KRAS/ERK/JUNB signaling suppresses differentiation regulator GATA6 in pancreatic cancer.The Journal of clinical investigation · 2026Article
- 19S proteasome loss regulates mitotic spindle assembly through a ubiquitin-independent degradation mechanism.Cell reports · 2025Article
- 19S proteasome loss causes monopolar spindles through ubiquitin-independent KIF11 degradation.bioRxiv : the preprint server for biology · 2025Article
- Epidermal growth factor receptor (EGFR) is a target of the tumor-suppressor E3 ligase FBXW7.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Genome-wide CRISPR/Cas9 screen reveals JunB downmodulation of HIV co-receptor CXCR4.Frontiers in microbiology · 2024Article
- New roles for AP-1/JUNB in cell cycle control and tumorigenic cell invasion via regulation of cyclin E1 and TGF-β2.Genome biology · 2022Article
- Ubiquitin-specific protease 28 deubiquitinates TCF7L2 to govern the action of the Wnt signaling pathway in hepatic carcinoma.Cancer science · 2022Article
- Article
- FGF7/FGFR2-JunB signalling counteracts the effect of progesterone in luminal breast cancer.Molecular oncology · 2022Article
- Systematic Discovery of FBXW7-Binding Phosphodegrons Highlights Mitogen-Activated Protein Kinases as Important Regulators of Intracellular Protein Levels.International journal of molecular sciences · 2022Article
- Description of CRISPR-Cas9 development and its prospects in human papillomavirus-driven cancer treatment.Frontiers in immunology · 2022Review
- Truncation of the TPR domain of OGT alters substrate and glycosite selection.Analytical and bioanalytical chemistry · 2021Article
- A Regulatory Loop of FBXW7-MYC-PLK1 Controls Tumorigenesis of MYC-Driven Medulloblastoma.Cancers · 2021Article
- AP-1 family transcription factors: a diverse family of proteins that regulate varied cellular activities in classical hodgkin lymphoma and ALK+ ALCL.Experimental hematology & oncology · 2021Review
- Lead DEAD/H box helicase biomarkers with the therapeutic potential identified by integrated bioinformatic approaches in lung cancer.Computational and structural biotechnology journal · 2021Article
- Tumor Suppressor FBXW7 and Its Regulation of DNA Damage Response and Repair.Frontiers in cell and developmental biology · 2021Review
- Regulation of cell cycle drivers by Cullin-RING ubiquitin ligases.Experimental & molecular medicine · 2020Review
- Review
- The ubiquitin-like modifier FAT10 interferes with SUMO activation.Nature communications · 2019Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
JunB, an activator protein-1 (AP-1) transcription factor component, acts either as a tumor suppressor or as an oncogene depending on the cell context. In particular, JunB is strongly upregulated in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL) where it enhances cell proliferation. Although its overexpression is linked to lymphomagenesis, the mechanisms whereby JunB promotes neoplastic growth are still largely obscure. Here, we show that JunB undergoes coordinated phosphorylation-dependent ubiquitylation during the G2 phase of the cell cycle. We characterized a critical consensus phospho-degron that controls JunB turnover and identified GSK3 and SCF(FBXW7) as, respectively, the kinase and the E3 ubiquitin ligase responsible for its degradation in G2. Pharmacological or genetic inactivation of the GSK3-FBXW7-JunB axis induced accumulation of JunB in G2/M and entailed transcriptional repression of the DNA helicase DDX11, leading to premature sister chromatid separation. This abnormal phenotype due to dysregulation of the GSK3β/JunB/DDX11 pathway is phenocopied in ALK-positive ALCL. Thus, our results reveal a novel mechanism by which mitosis progression and chromatid cohesion are regulated through GSK3/SCF(FBXW7)-mediated proteolysis of JunB, and suggest that JunB proteolysis in G2 is an essential step in maintaining genetic fidelity during mitosis.
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