Evidence map›Paper›PMID 12426378›Full record

ArticleThe EMBO journal2002

Dissection of c-MOS degron.

Jun Sheng, Akiko Kumagai, William G Dunphy, Alexander Varshavsky

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. BMI1, a new target of CK2α.Molecular cancer · 2017
    Article
  6. Article
  7. Article
  8. Dephosphorylation-induced ubiquitination and degradation of FMRP in dendrites: a role in immediate early mGluR-stimulated translation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  9. Article
  10. Article
  11. Review
  12. Discovery of cellular regulation by protein degradation.The Journal of biological chemistry · 2008
    Article
  13. Article
  14. Mechanistic studies of the mitotic activation of Mos.Molecular and cellular biology · 2006
    Article
  15. Article
  16. Article
  17. Article
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

4 authors at 1 institution in 1 country.

Jun ShengDivision of Biology, 147-75, California Institute of Technology, 1200 East California Blvd, Pasadena, CA 91125, USA.
Akiko Kumagai
William G Dunphy
Alexander Varshavsky
California Institute of Technology · US

Funding

The Functions, Mechanisms, and Regulation of N-Terminal ArginylationR01GM031530 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ALEXANDER J VARSHAVSKY · 1985 to 2026
$14.5M
Ubiquitin Ligases, Mechanisms and Functions of the N-End Rule PathwayR01DK039520 · NIDDK · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI VARSHAVSKY, ALEXANDER J · 1988 to 2025
$10.0M
MECHANICS AND FUNCTIONS OF THE N-END RULE PATHWAYR37DK039520 · NIDDK · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI VARSHAVSKY, ALEXANDER J · 1998 to 2007
$4.4M
ENZYMOLOGY OF MITOSIS PROMOTING FACTOR (MPF)R01GM043974 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI DUNPHY, WILLIAM G · 1990 to 2022
$4.0M
Enzymology of Mitosis Promoting Factor (MPF)R37GM043974 · NIGMS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI DUNPHY, WILLIAM G · 2002 to 2011
$4.0M
Ubiquitin Ligases, Mechanisms and Functions of the N-End Rule PathwayR56DK039520 · NIDDK · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI VARSHAVSKY, ALEXANDER J · 2008 to 2008
$161k
NIDDK NIH HHS DK 39520NIDDK NIH HHS R01 DK039520NIDDK NIH HHS R37 DK039520NIDDK NIH HHS R56 DK039520NIGMS NIH HHS GM 31530NIGMS NIH HHS GM 43974NIGMS NIH HHS R01 GM031530NIGMS NIH HHS R01 GM043974NIGMS NIH HHS R37 GM043974
6 · The paper itself

Abstract

c-MOS, a MAP kinase kinase kinase, is a regulator of oocyte maturation. The concentration of c-MOS is controlled in part through its conditional degradation. Previous studies proposed the "second-codon rule", according to which the N-terminal proline (Pro) of c-MOS is a destabilizing residue that targets c-MOS for degradation. We analyzed the degradation signal (degron) of c-MOS in Xenopus oocytes, found it to be a portable degron, and demonstrated that, contrary to the model above, the N-terminal Pro residue of c-MOS is entirely dispensable for its degradation if Ser-2 (encoded Ser-3) of c-MOS is replaced by a small non-phosphorylatable residue such as Gly. The dependence of c-MOS degradation on N-terminal Pro is shown to be caused by a Pro-mediated downregulation of the net phosphorylation of Ser-2, a modification that halts c-MOS degradation in oocytes. Thus, the N-terminal Pro residue of c-MOS is not a recognition determinant for a ubiquitin ligase, in agreement with earlier evidence that Pro is a stabilizing residue in the N-end rule.

Indexed as

3T3 CellsAmino Acid SequenceAmino Acid SubstitutionAnimalsEndopeptidasesFibroblastsGenes, mosLigasesMiceMicroinjectionsMolecular Sequence DataOocytesPhosphorylationPhosphoserineProgesteroneProlineEndopeptidasesLigasesPhosphoserineProgesteroneProlineProto-Oncogene Proteins c-mosRecombinant Fusion Proteins

Identifiers

PMID12426378
PMCPMC137215
OpenAlexW2140558722

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.