Evidence map›Paper›PMID 28096334›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Role of CCT chaperonin in the disassembly of mitotic checkpoint complexes.

Sharon Kaisari, Danielle Sitry-Shevah, Shirly Miniowitz-Shemtov, Adar Teichner, Avram Hershko

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. 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
3.3field-weighted citation impact, top 8% 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, 52 citations in OpenAlex.

  1. Article
  2. Chaperonin in health and disease.Molecular biomedicine · 2026
    Review
  3. Article
  4. Role of TRIP13 in human cancer development.Molecular biology reports · 2024
    Review
  5. Review
  6. Role of ubiquitin-protein ligase UBR5 in the disassembly of mitotic checkpoint complexes.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. ThemicroPublication biology · 2022
    Article
  9. The TRiCky Business of Protein Folding in Health and Disease.Frontiers in cell and developmental biology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Polycomb RequiresFrontiers in cell and developmental biology · 2021
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Sharon KaisariUnit of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 31096, Israel.
Danielle Sitry-ShevahUnit of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 31096, Israel.
Shirly Miniowitz-ShemtovUnit of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 31096, Israel.
Adar TeichnerUnit of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 31096, Israel.
Avram HershkoUnit of Biochemistry, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa 31096, Israel hershko@tx.technion.ac.il.
Technion – Israel Institute of Technology · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitotic checkpoint system prevents premature separation of sister chromatids in mitosis and thus ensures the fidelity of chromosome segregation. When this checkpoint is active, a mitotic checkpoint complex (MCC), composed of the checkpoint proteins Mad2, BubR1, Bub3, and Cdc20, is assembled. MCC inhibits the ubiquitin ligase anaphase promoting complex/cyclosome (APC/C), whose action is necessary for anaphase initiation. When the checkpoint signal is turned off, MCC is disassembled, a process required for exit from checkpoint-arrested state. Different moieties of MCC are disassembled by different ATP-requiring processes. Previous work showed that Mad2 is released from MCC by the joint action of the TRIP13 AAA-ATPase and the Mad2-binding protein p31

Indexed as

Adenosine TriphosphateAnimalsATPases Associated with Diverse Cellular ActivitiesCdc20 ProteinsCell Cycle ProteinsChaperonin Containing TCP-1HeLa CellsHumansMad2 ProteinsM Phase Cell Cycle CheckpointsProtein Serine-Threonine KinasesRecombinant ProteinsSf9 CellsSpindle ApparatusSpodopteraStaurosporineAdenosine TriphosphateATPases Associated with Diverse Cellular ActivitiesBUB1 protein, humanCDC20 protein, humanCdc20 ProteinsCell Cycle ProteinsChaperonin Containing TCP-1MAD2L1 protein, humanMad2 ProteinsProtein Serine-Threonine KinasesRecombinant ProteinsStaurosporineTRIP13 protein, humancell cycleprotein degradationubiquitin

Identifiers

PMID28096334
PMCPMC5293070
OpenAlexW2574793523

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.