Evidence map›Paper›PMID 11709728›Full record

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.

C Acquaviva, F Brockly, P Ferrara, G Bossis, C Salvat, I Jariel-Encontre, M Piechaczyk

Abstract read
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. GnRH increases c-Fos half-life contributing to higher FSHβ induction.Molecular endocrinology (Baltimore, Md.) · 2013
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Regulation of DeltaFosB stability by phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006
    Article
  13. Article
  14. Article
  15. Essential role of RSK2 in c-Fos-dependent osteosarcoma development.The Journal of clinical investigation · 2005
    Article
  16. Article
  17. Article
  18. Cancer genomics & proteomics
    Article
  19. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

C AcquavivaInstitute of Molecular Genetics, UMR5535/IFR24, CNRS, 1919, route de Mende, 34293-Montpellier Cedex 05, France.
F Brockly
P Ferrara
G Bossis
C Salvat
I Jariel-Encontre
M Piechaczyk
Centre National de la Recherche Scientifique · FRInstitut de Génétique Moléculaire de Montpellier · FRTexas Medical Board · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

3T3 CellsAmino Acid MotifsAmino AcidsAmino Acid SequenceAnimalsBlotting, NorthernBlotting, WesternCysteine EndopeptidasesGene DeletionHumansMiceMice, Inbred BALB CModels, GeneticMolecular Sequence DataMultienzyme ComplexesMultigene FamilyAmino AcidsCysteine EndopeptidasesMultienzyme ComplexesPeptidesProteasome Endopeptidase ComplexProto-Oncogene Proteins c-fosRNA, Messenger

Identifiers

PMID11709728
OpenAlexW2318733877

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.