ArticleOncogene2001
Identification of a C-terminal tripeptide motif involved in the control of rapid proteasomal degradation of c-Fos proto-oncoprotein during the G(0)-to-S phase transition.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- Regulation of PEST-containing nuclear proteins in cancer cells: implications for cancer biology and therapy.Frontiers in oncology · 2025Review
- Recurrent FOSL1 rearrangements in desmoplastic fibroblastoma.The Journal of pathology · 2023Article
- Age-Dependent FOSB/ΔFOSB Response to Acute and Chronic Stress in the Extended Amygdala, Hypothalamic Paraventricular, Habenular, Centrally-Projecting Edinger-Westphal, and Dorsal Raphe Nuclei in Male Rats.Frontiers in aging neuroscience · 2022Article
- 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
- Signal-dependent fra-2 regulation in skeletal muscle reserve and satellite cells.Cell death & disease · 2013Article
- GnRH increases c-Fos half-life contributing to higher FSHβ induction.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Proline-mediated proteasomal degradation of the prostate-specific tumor suppressor NKX3.1.The Journal of biological chemistry · 2012Article
- A 19S proteasomal subunit cooperates with an ERK MAPK-regulated degron to regulate accumulation of Fra-1 in tumour cells.Oncogene · 2012Article
- Site-specific methionine oxidation initiates calmodulin degradation by the 20S proteasome.Biochemistry · 2009Article
- Regulation of retention of FosB intron 4 by PTB.PloS one · 2007Article
- Ubiquitin-independent proteasomal degradation of Fra-1 is antagonized by Erk1/2 pathway-mediated phosphorylation of a unique C-terminal destabilizer.Molecular and cellular biology · 2007Article
- Regulation of DeltaFosB stability by phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Role of N-terminal residues in the ubiquitin-independent degradation of human thymidylate synthase.The Biochemical journal · 2006Article
- Down-regulation of c-Fos/c-Jun AP-1 dimer activity by sumoylation.Molecular and cellular biology · 2005Article
- Essential role of RSK2 in c-Fos-dependent osteosarcoma development.The Journal of clinical investigation · 2005Article
- c-Fos proto-oncoprotein is degraded by the proteasome independently of its own ubiquitinylation in vivo.Molecular and cellular biology · 2003Article
- The structural determinants responsible for c-Fos protein proteasomal degradation differ according to the conditions of expression.Oncogene · 2003Article
- Article
- Neoplasia-associated Chromosome Translocations Resulting in Gene Truncation.Cancer genomics & proteomicsReview
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Fos proto-oncoprotein is rapidly and transiently expressed in cells undergoing the G(0)-to-S phase transition in response to stimulation for growth by serum. Under these conditions, the rapid decay of the protein occurring after induction is accounted for by efficient recognition and degradation by the proteasome. PEST motifs are sequences rich in Pro, Glu, Asp, Ser and Thr which have been proposed to constitute protein instability determinants. c-Fos contains three such motifs, one of which comprises the C-terminal 20 amino acids and has already been proposed to be the major determinant of c-Fos instability. Using site-directed mutagenesis and an expression system reproducing c-fos gene transient expression in transfected cells, we have analysed the turnover of c-Fos mutants deleted of the various PEST sequences in synchronized mouse embryo fibroblasts. Our data showed no role for the two internal PEST motifs in c-Fos instability. However, deletion of the C-terminal PEST region led to only a twofold stabilization of the protein. Taken together, these data indicate that c-Fos instability during the G0-to-S phase transition is governed by a major non-PEST destabilizer and a C-terminal degradation-accelerating element. Further dissection of c-Fos C-terminal region showed that the degradation-accelerating effect is not contributed by the whole PEST sequence but by a short PTL tripeptide which cannot be considered as a PEST motif and which can act in the absence of any PEST environment. Interestingly, the PTL motif is conserved in other members of the fos multigene family. Nevertheless, its contribution to protein instability is restricted to c-Fos suggesting that the mechanisms whereby the various Fos proteins are broken down are, at least partially, different. MAP kinases-mediated phosphorylation of two serines close to PTL, which are both phosphorylated all over the G(0)-to-S phase transition, have been proposed by others to stabilize c-Fos protein significantly. We, however, showed that the PTL motif does not exert its effect by counteracting a stabilizing effect of these phosphorylations under our experimental conditions.
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