Evidence map›Paper›PMID 30485802›Full record

ArticleCell reports2018

Deletion of APC7 or APC16 Allows Proliferation of Human Cells without the Spindle Assembly Checkpoint.

Thomas Wild, Magda Budzowska, Susanne Hellmuth, Susana Eibes, Gopal Karemore, Marin Barisic, Olaf Stemmann, Chunaram Choudhary

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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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 4 institutions in 2 countries.

Thomas WildProteomics Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark.
Magda BudzowskaProteomics Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark; Center for Chromosome Stability (CCS), Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark.
Susanne HellmuthChair of Genetics, University of Bayreuth, Universitätsstraße 30, 95440 Bayreuth, Germany.
Susana EibesDanish Cancer Society Research Center, Cell Division Laboratory, Strandboulevarden 49, 2100 Copenhagen, Denmark.
Gopal KaremoreProtein Imaging Platform, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark.
Marin BarisicDanish Cancer Society Research Center, Cell Division Laboratory, Strandboulevarden 49, 2100 Copenhagen, Denmark; Department of Cellular and Molecular Medicine, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.
Olaf StemmannChair of Genetics, University of Bayreuth, Universitätsstraße 30, 95440 Bayreuth, Germany.
Chunaram ChoudharyProteomics Program, Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark. Electronic address: chuna.choudhary@cpr.ku.dk.
Novo Nordisk Foundation · DKDanish Cancer Society · DKUniversity of Bayreuth · DEUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The multisubunit ubiquitin ligase APC/C (anaphase-promoting complex/cyclosome) is essential for mitosis by promoting timely degradation of cyclin B1. APC/C is tightly regulated by the spindle assembly checkpoint (SAC), which involves MPS1 and MAD2-dependent temporal inhibition of APC/C. We analyzed the contribution of the APC/C subunits APC7 and APC16 to APC/C composition and function in human cells. APC16 is required for APC7 assembly into APC/C, whereas APC16 assembles independently of APC7. APC7 and APC16 knockout cells display no major defects in mitotic progression, cyclin B1 degradation, or SAC response, but APC/C lacking these two subunits shows reduced ubiquitylation activity in vitro. Strikingly, deletion of APC7 or APC16 is sufficient to provide synthetic viability to MAD2 deletion. ΔAPC7ΔMAD2 cells display accelerated mitosis and require SAC-independent MPS1 function for genome stability. These findings reveal that the composition of APC/C critically influences the importance of the SAC in humans.

Indexed as

M Phase Cell Cycle CheckpointsAnaphase-Promoting Complex-CyclosomeApc7 Subunit, Anaphase-Promoting Complex-CyclosomeCell Cycle ProteinsCell ProliferationHCT116 CellsHeLa CellsHumansMad2 ProteinsMitosisUbiquitinationANAPC16 protein, humanANAPC7 protein, humanAnaphase-Promoting Complex-CyclosomeApc7 Subunit, Anaphase-Promoting Complex-CyclosomeCell Cycle ProteinsMAD2L1 protein, humanMad2 ProteinsAPC16APC7APC/CMAD2mass spectrometrymitosisMPS1synthetic viability

Identifiers

PMID30485802
PMCPMC6289045
OpenAlexW2902882072

What OpenQuestion holds

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Registered trials

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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.