ArticleOncogene2011
COP9 signalosome subunit 6 stabilizes COP1, which functions as an E3 ubiquitin ligase for 14-3-3σ.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 54 citations in OpenAlex.
- Induced ubiquitination of the partially disordered estrogen receptor alpha via a 14-3-3 directed molecular glue-PROTAC.Nature communications · 2026Article
- Interaction of CSN4 to DDB1 regulates its stability and function in DNA damage signaling.Cellular and molecular life sciences : CMLS · 2026Article
- COP9 Signalosome's Role in Plant Defense Mechanisms.Plants (Basel, Switzerland) · 2025Review
- Distinct roles of Constitutive Photomorphogenesis Protein 1 homolog (COP1) in human hepatocyte models.Frontiers in molecular biosciences · 2025Article
- Friend or foe? Reciprocal regulation between E3 ubiquitin ligases and deubiquitinases.Biochemical Society transactions · 2024Review
- In Silico Studies on GCP-Lys-OMe as a Potential 14-3-3σ Homodimer Stabilizer.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Genetic Dissection of Light-Regulated Adventitious Root Induction inInternational journal of molecular sciences · 2022Article
- The Involvement of Ubiquitination Machinery in Cell Cycle Regulation and Cancer Progression.International journal of molecular sciences · 2021Review
- CSN6 promotes melanoma proliferation and metastasis by controlling the UBR5-mediated ubiquitination and degradation of CDK9.Cell death & disease · 2021Article
- 14-3-3σ and Its Modulators in Cancer.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Regulation of p53 by the 14-3-3 protein interaction network: new opportunities for drug discovery in cancer.Cell death discovery · 2020Review
- EGF Relays Signals to COP1 and Facilitates FOXO4 Degradation to Promote Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- CSN6: a promising target for cancer prevention and therapy.Histology and histopathology · 2020Review
- Correlation of constitutive photomorphogenic 1 (COP1) and p27 tumor suppressor protein expression in ovarian cancer.Genes & genomics · 2019Article
- CSN6 promotes tumorigenesis of gastric cancer by ubiquitin-independent proteasomal degradation of p16Cancer biology & medicine · 2019Article
- Role of the COP9 Signalosome (CSN) in Cardiovascular Diseases.Biomolecules · 2019Review
- CSN6 expression is associated with pancreatic cancer progression and predicts poor prognosis.Cancer biology & therapy · 2019Article
- CSN6 Promotes the Migration and Invasion of Cervical Cancer Cells by Inhibiting Autophagic Degradation of Cathepsin L.International journal of biological sciences · 2019Article
- Downregulation of CSN6 attenuates papillary thyroid carcinoma progression by reducing Wnt/β-catenin signaling and sensitizes cancer cells to FH535 therapy.Cancer medicine · 2018Article
- 14-3-3σ downregulation suppresses ICC metastasis via impairing migration, invasion, and anoikis resistance of ICC cells.Cancer biomarkers : section A of Disease markers · 2017Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
Abstract
14-3-3σ, a gene upregulated by p53 in response to DNA damage, exists as part of a positive-feedback loop, which activates p53 and is a human cancer epithelial marker downregulated in various cancer types. 14-3-3σ levels are critical for maintaining p53 activity in response to DNA damage and regulating signal mediators such as Akt. In this study, we identify mammalian constitutive photomorphogenic 1 (COP1) as a novel E3 ubiquitin ligase for targeting 14-3-3σ through proteasomal degradation. We show for the first time that COP9 signalosome subunit 6 (CSN6) associates with COP1 and is involved in 14-3-3σ ubiquitin-mediated degradation. Mechanistic studies show that CSN6 expression leads to stabilization of COP1 through reducing COP1 self-ubiquitination and decelerating COP1's turnover rate. We also show that CSN6-mediated 14-3-3σ ubiquitination is compromised when COP1 is knocked down. Thus, CSN6 mediates 14-3-3σ ubiquitination through enhancing COP1 stability. Subsequently, we show that CSN6 causes 14-3-3σ downregulation, thereby activating Akt and promoting cell survival. Also, CSN6 overexpression leads to increased cell growth, transformation and promotes tumorigenicity. Significantly, 14-3-3σ expression can correct the abnormalities mediated by CSN6 expression. These data suggest that the CSN6-COP1 axis is involved in 14-3-3σ degradation, and that deregulation of this axis will promote cell growth and tumorigenicity.
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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.