ArticleMolecular and cellular biology2003
c-Fos proto-oncoprotein is degraded by the proteasome independently of its own ubiquitinylation in vivo.
Article in Molecular and cellular biology, 2003. 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, 74 citations in OpenAlex.
- Proteasomal surveillance of exposed cysteines.bioRxiv : the preprint server for biology · 2026Article
- Hydrophobic Tag Protein Degraders: An Emerging Therapeutic Strategy for Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Proteasomal control of transcription factors: mechanisms, regulation and dysregulation.Cellular and molecular life sciences : CMLS · 2026Review
- Truncated FOS impairs osteogenic differentiation and induces prostaglandin and NFκB signalling in an in vitro cell-of-origin model for osteoid osteoma and osteoblastoma.The Journal of pathology · 2026Article
- Oncogenic KRAS/ERK/JUNB signaling suppresses differentiation regulator GATA6 in pancreatic cancer.The Journal of clinical investigation · 2026Article
- Degrons: defining the rules of protein degradation.Nature reviews. Molecular cell biology · 2025Review
- Mechanisms of ubiquitin-independent proteasomal degradation and their roles in age-related neurodegenerative disease.Frontiers in cell and developmental biology · 2024Review
- The midnolin-proteasome pathway catches proteins for ubiquitination-independent degradation.Science (New York, N.Y.) · 2023Article
- Ubiquitin-independent proteasomal degradation driven by C-degron pathways.Molecular cell · 2023Article
- Contribution of the Transcription Factors Sp1/Sp3 and AP-1 toInternational journal of molecular sciences · 2021Article
- The proteasome and its role in the nervous system.Cell chemical biology · 2021Review
- Small Molecule Modulation of Proteasome Assembly.Biochemistry · 2018Article
- Review
- Functional analyses of a human vascular tumor FOS variant identify a novel degradation mechanism and a link to tumorigenesis.The Journal of biological chemistry · 2017Article
- A simple toolset to identify endogenous post-translational modifications for a target protein: a snapshot of the EGFR signaling pathway.Bioscience reports · 2017Article
- c-Fos Protects Neurons Through a Noncanonical Mechanism Involving HDAC3 Interaction: Identification of a 21-Amino Acid Fragment with Neuroprotective Activity.Molecular neurobiology · 2016Article
- GSK3-SCF(FBXW7) targets JunB for degradation in G2 to preserve chromatid cohesion before anaphase.Oncogene · 2013Article
- GnRH increases c-Fos half-life contributing to higher FSHβ induction.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Barriers to transmission of transcriptional noise in a c-fos c-jun pathway.Molecular systems biology · 2013Article
- Calcineurin mediates the gonadotropin-releasing hormone effect on expression of both subunits of the follicle-stimulating hormone through distinct mechanisms.Molecular and cellular biology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prior ubiquitinylation of the unstable c-Fos proto-oncoprotein is thought to be required for recognition and degradation by the proteasome. Contradicting this view, we report that, although c-Fos can form conjugates with ubiquitin in vivo, nonubiquitinylatable c-Fos mutants show regulated degradation identical to that of the wild-type protein in living cells under two classical conditions of study: transient c-fos gene expression during the G(0)/G(1) phase transition upon stimulation by mitogens and constitutive expression during asynchronous growth. Moreover, c-Fos destruction during the G(0)/G(1) phase transition is unusual because it depends on two distinct but cumulative mechanisms. We report here that one mechanism involves a C-terminal destabilizer which does not need an active ubiquitin cycle, whereas the other involves an N-terminal destabilizer dependent on ubiquitinylation of an upstream c-Fos breakdown effector. In addition to providing new insights into the mechanisms of c-Fos protein destruction, an important consequence of our work is that ubiquitinylation-dependent proteasomal degradation claimed for a number of proteins should be reassessed on a new experimental basis.
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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.