Evidence map›Paper›PMID 39018254›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

CCDC68 Maintains Mitotic Checkpoint Activation by Promoting CDC20 Integration into the MCC.

Qi Li, Qingzhou Chen, Tao Zheng, Fulin Wang, Junlin Teng, Haining Zhou, Jianguo Chen

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. CCDC68 Maintains Mitotic Checkpoint Activation by Promoting CDC20 Integration into the MCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    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

7 authors.

Qi LiKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.
Qingzhou ChenKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.
Tao ZhengKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.
Fulin WangKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.
Junlin TengKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.
Haining ZhouKey Laboratory of Epigenetic Regulation and Intervention, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Jianguo ChenKey Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing, 100871, China.ORCID 0000-0002-8406-011X

Funding

Chinese Academy of Sciences (CAS) Strategic Priority Research Program XDB37010100Key Technologies Research and Development Program 2016YFA0100501National Natural Science Foundation of China 31830110National Natural Science Foundation of China 32130024National Natural Science Foundation of China 32370635
6 · The paper itself

Abstract

The spindle assembly checkpoint (SAC) ensures chromosome segregation fidelity by manipulating unattached kinetochore-dependent assembly of the mitotic checkpoint complex (MCC). The MCC binds to and inhibits the anaphase promoting complex/cyclosome (APC/C) to postpone mitotic exit. However, the mechanism by which unattached kinetochores mediate MCC formation is not yet fully understood. Here, it is shown that CCDC68 is an outer kinetochore protein that preferentially localizes to unattached kinetochores. Furthermore, CCDC68 interacts with the SAC factor CDC20 to inhibit its autoubiquitination and MCC disassembly. Therefore, CCDC68 restrains APC/C activation to ensure a robust SAC and allow sufficient time for chromosome alignment, thus ensuring chromosomal stability. Hence, the study reveals that CCDC68 is required for CDC20-dependent MCC stabilization to maintain mitotic checkpoint activation.

Indexed as

Cdc20 ProteinsKinetochoresM Phase Cell Cycle CheckpointsAnaphase-Promoting Complex-CyclosomeCell Cycle ProteinsChromosome SegregationHeLa CellsHumansMitosisTumor Suppressor ProteinsAnaphase-Promoting Complex-CyclosomeCCDC68 protein, humanCDC20 protein, humanCdc20 ProteinsCell Cycle ProteinsTumor Suppressor ProteinsCCDC68CDC20kinetochoremitotic checkpoint complexspindle assembly checkpoint

Identifiers

PMID39018254
PMCPMC11425217

What OpenQuestion holds

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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.