ArticleCancer research2006
COOH-terminal Src kinase-mediated c-Jun phosphorylation promotes c-Jun degradation and inhibits cell transformation.
Article in Cancer research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- AP1 Transcription Factor in the Regulation of the Urokinase Plasminogen Activation System.Biomolecules · 2026Review
- c-Jun inhibition mitigates chemotherapy-induced neurotoxicity in iPSC-derived sensory neurons.Cell death discovery · 2025Article
- JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025Review
- CSK-mediated signalling by integrins in cancer.Frontiers in cell and developmental biology · 2023Review
- p38-dependent c-Jun degradation contributes to reduced PGE2 production in sodium orthovanadate-treated macrophages.BMB reports · 2022Article
- Article
- Enzyme-substrate relationships in the ubiquitin system: approaches for identifying substrates of ubiquitin ligases.Cellular and molecular life sciences : CMLS · 2017Review
- Cdk3-promoted epithelial-mesenchymal transition through activating AP-1 is involved in colorectal cancer metastasis.Oncotarget · 2016Article
- Article
- TPA-induced cell transformation provokes a complex formation between Pin1 and 90 kDa ribosomal protein S6 kinase 2.Molecular and cellular biochemistry · 2012Article
- Regulation of the SRC family kinases by Csk.International journal of biological sciences · 2012Review
- Cyclin-dependent kinase-3-mediated c-Jun phosphorylation at Ser63 and Ser73 enhances cell transformation.Cancer research · 2009Article
- Antiproliferative effect of sulindac in colonic neoplasia prevention: role of COOH-terminal Src kinase.Molecular cancer therapeutics · 2008Article
- The functional contrariety of JNK.Molecular carcinogenesis · 2007Review
- Methylation-controlled J protein promotes c-Jun degradation to prevent ABCB1 transporter expression.Molecular and cellular biology · 2007Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The oncoprotein c-Jun is a component of the activator protein-1 transcription factor complex, which is involved in cellular proliferation, transformation, and death. The stabilization of c-Jun is critically important for its function. The phosphorylation of c-Jun by c-Jun NH(2)-terminal kinase 1 and extracellular signal-regulated protein kinases reduces c-Jun ubiquitination resulting in increased stabilization of c-Jun. In this report, we showed that COOH-terminal Src kinase (CSK) binds with and phosphorylates c-Jun at Y26 and Y170. Phosphorylation of c-Jun by CSK, in opposition to c-Jun NH(2)-terminal kinase 1 and extracellular signal-regulated protein kinases, promoted c-Jun degradation and reduced stability. By promoting c-Jun degradation, CSK helps to maintain a low steady-state level of c-Jun, thereby inhibiting activator protein-1 activity and cell transformation caused by c-Jun. These results indicated that this function of CSK controls cell proliferation under normal growth conditions and may have implications for CSK loss of function in carcinogenesis.
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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.