Evidence map›Paper›PMID 18504434›Full record

ArticleOncogene2008

Chfr interacts and colocalizes with TCTP to the mitotic spindle.

A Burgess, J-C Labbé, S Vigneron, N Bonneaud, J M Strub, A Van Dorsselaer, T Lorca, A Castro

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

31 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Tctp, a unique Ing5-binding partner, inhibits the chromatin binding of Enok inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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  8. Review
  9. Article
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  16. Article
  17. Degrading Claspin away with Cdh1 and Cyclin A.Cell cycle (Georgetown, Tex.) · 2015
    Article
  18. Article
  19. Review
  20. TCTP overexpression is associated with the development and progression of glioma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013
    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

8 authors at 3 institutions in 1 country.

A BurgessUniversités Montpellier 2 et 1, Centre de Recherche de Biochimie Macromoléculaire, CNRS UMR 5237, IFR 122, Labellisée Ligue Nationale Contre le Cancer, Montpellier Cedex, France.
J-C Labbé
S Vigneron
N Bonneaud
J M Strub
A Van Dorsselaer
T Lorca
A Castro
Centre de Recherche en Biologie cellulaire de Montpellier · FRCentre National de la Recherche Scientifique · FRInstitut Pluridisciplinaire Hubert Curien · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chfr is a checkpoint protein that plays an important function in cell cycle progression and tumor suppression, although its exact role and regulation are unclear. Previous studies have utilized overexpression of Chfr to determine the signaling pathway of this protein in vivo. In this study, we demonstrate, by using three different antibodies against Chfr, that the endogenous and highly overexpressed ectopic Chfr protein is localized and regulated differently in cells. Endogenous and lowly expressed ectopic Chfr are cytoplasmic and localize to the spindle during mitosis. Higher expression of ectopic Chfr correlates with a shift in the localization of this protein to the nucleus/PML bodies, and with a block of cell proliferation. In addition, endogenous and lowly expressed ectopic Chfr is stable throughout the cell cycle, whereas when highly expressed, ectopic Chfr is actively degraded during S-G2/M phases in an autoubiquitination and proteasome-dependent manner. A two-hybrid screen identified TCTP as a possible Chfr-interacting partner. Biochemical analysis with the endogenous proteins confirmed this interaction and identified beta-tubulin as an additional partner for Chfr, supporting the mitotic spindle localization of Chfr. The Chfr-TCTP interaction was stable throughout the cell cycle, but it could be diminished by the complete depolymerization of the microtubules, providing a possible mechanism where Chfr could be the sensor that detects microtubule disruption and then activates the prophase checkpoint.

Indexed as

AnimalsBiomarkers, TumorCell CycleCell Cycle ProteinsHeLa CellsHumansMicrotubulesNeoplasm ProteinsPhosphorylationPoly-ADP-Ribose Binding ProteinsSpindle ApparatusTubulinTumor Protein, Translationally-Controlled 1UbiquitinationUbiquitin-Protein LigasesXenopusBiomarkers, TumorCell Cycle ProteinsCHFR protein, humanNeoplasm ProteinsPoly-ADP-Ribose Binding ProteinsTPT1 protein, humanTubulinTumor Protein, Translationally-Controlled 1Ubiquitin-Protein Ligases

Identifiers

PMID18504434
OpenAlexW1967641707

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.