ArticleMolecular and cellular biology2010
c-Fos proteasomal degradation is activated by a default mechanism, and its regulation by NAD(P)H:quinone oxidoreductase 1 determines c-Fos serum response kinetics.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- 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
- Insights into the cellular function and mechanism of action of quinone reductase 2 (NQO2).The Biochemical journal · 2025Review
- NQO1 regulates cell cycle progression at the G2/M phase.Theranostics · 2023Article
- Protection of c-Fos from autophagic degradation by PRMT1-mediated methylation fosters gastric tumorigenesis.International journal of biological sciences · 2023Article
- Targeting HIF-1α Function in Cancer through the Chaperone Action of NQO1: Implications of Genetic Diversity of NQO1.Journal of personalized medicine · 2022Review
- Identification of MAGEC2/CT10 as a High Calcium-Inducible Gene in Triple-Negative Breast Cancer.Frontiers in endocrinology · 2022Article
- NQO1 Binds and Supports SIRT1 Function.Frontiers in pharmacology · 2021Article
- Transcription factor Ets-2 regulates the expression of key lymphotropic factors.Molecular biology reports · 2020Article
- NQO1 potentiates apoptosis evasion and upregulates XIAP via inhibiting proteasome-mediated degradation SIRT6 in hepatocellular carcinoma.Cell communication and signaling : CCS · 2019Article
- Cancer-associated variants of human NQO1: impacts on inhibitor binding and cooperativity.Bioscience reports · 2019Article
- Small Molecule Modulation of Proteasome Assembly.Biochemistry · 2018Article
- Oncogenic addiction to high 26S proteasome level.Cell death & disease · 2018Article
- c-Fos mapping of brain regions activated by multi-modal and electric foot shock stress.Neurobiology of stress · 2018Article
- 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
- The NS1 protein of H5N6 feline influenza virus inhibits feline beta interferon response by preventing NF-κB and IRF3 activation.Developmental and comparative immunology · 2017Article
- A Signaling Network Controlling Androgenic Repression of c-Fos Protein in Prostate Adenocarcinoma Cells.The Journal of biological chemistry · 2016Article
- Compromising the 19S proteasome complex protects cells from reduced flux through the proteasome.eLife · 2015Article
- Proteins directly interacting with mammalian 20S proteasomal subunits and ubiquitin-independent proteasomal degradation.Biomolecules · 2014Review
- Regulating the 20S proteasome ubiquitin-independent degradation pathway.Biomolecules · 2014Review
- Calpain-generated natural protein fragments as short-lived substrates of the N-end rule pathway.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The short-lived proto-oncoprotein c-Fos is a component of the activator protein 1 (AP-1) transcription factor. A large region of c-Fos is intrinsically unstructured and susceptible to a recently characterized proteasomal ubiquitin-independent degradation (UID) pathway. UID is active by a default mechanism that is inhibited by NAD(P)H:quinone oxidoreductase 1 (NQO1), a 20S proteasome gatekeeper. Here, we show that NQO1 binds and induces robust c-Fos accumulation by blocking the UID pathway. c-Jun, a partner of c-Fos, also protects c-Fos from proteasomal degradation by default. Our findings suggest that NQO1 protects monomeric c-Fos from proteasomal UID, a function that is fulfilled later by c-Jun. We show that this process regulates c-Fos homeostasis (proteostasis) in response to serum stimulation, phosphorylation, nuclear translocation, and transcription activity. In addition, we show that NQO1 is important to ensure immediate c-Fos accumulation in response to serum, since a delayed response was observed under low NQO1 expression. These data suggest that in vivo, protein unstructured regions determine the kinetics and the homeostasis of regulatory proteins. Our data provide evidence for another layer of regulation of key regulatory proteins that functions at the level of protein degradation and is designed to ensure optimal formation of functional complexes such as AP-1.
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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.