ArticleThe Journal of biological chemistry2011
Orderly inactivation of the key checkpoint protein mitotic arrest deficient 2 (MAD2) during mitotic progression.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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.
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.
Who cites it
20 citing papers in PubMed.
- Coregulation of NDC80 Complex Subunits Determines the Fidelity of the Spindle-Assembly Checkpoint and Mitosis.Molecular cancer research : MCR · 2024Article
- Cyclin A-CDK1 suppresses the expression of the CDK1 activator CDC25A to safeguard timely mitotic entry.The Journal of biological chemistry · 2023Article
- Mitotic slippage is determined by p31Oncogene · 2020Article
- Article
- Mad2 Overexpression Uncovers a Critical Role for TRIP13 in Mitotic Exit.Cell reports · 2017Article
- Phosphorylation of EB2 by Aurora B and CDK1 ensures mitotic progression and genome stability.Nature communications · 2016Article
- The mitotic checkpoint complex (MCC): looking back and forth after 15 years.AIMS molecular science · 2016Article
- The cilia-regulated proteasome and its role in the development of ciliopathies and cancer.Cilia · 2016Review
- Co-inhibition of polo-like kinase 1 and Aurora kinases promotes mitotic catastrophe.Oncotarget · 2015Article
- SGO1C is a non-functional isoform of Shugoshin and can disrupt sister chromatid cohesion by interacting with PP2A-B56.Cell cycle (Georgetown, Tex.) · 2015Article
- Panta rhei: the APC/C at steady state.The Journal of cell biology · 2013Review
- APC15 mediates CDC20 autoubiquitylation by APC/C(MCC) and disassembly of the mitotic checkpoint complex.Nature structural & molecular biology · 2012Article
- The APC/C subunit Mnd2/Apc15 promotes Cdc20 autoubiquitination and spindle assembly checkpoint inactivation.Molecular cell · 2012Article
- Depletion of p31comet protein promotes sensitivity to antimitotic drugs.The Journal of biological chemistry · 2012Article
- Checkpoint-independent stabilization of kinetochore-microtubule attachments by Mad2 in human cells.Current biology : CB · 2012Article
- Cohesion fatigue explains why pharmacological inhibition of the APC/C induces a spindle checkpoint-dependent mitotic arrest.PloS one · 2012Article
- p31comet-mediated extraction of Mad2 from the MCC promotes efficient mitotic exit.Journal of cell science · 2011Article
- Defining pathways of spindle checkpoint silencing: functional redundancy between Cdc20 ubiquitination and p31(comet).Molecular biology of the cell · 2011Article
- APC15 drives the turnover of MCC-CDC20 to make the spindle assembly checkpoint responsive to kinetochore attachment.Nature cell biology · 2011Article
- CHFR binds to and regulates MAD2 in the spindle checkpoint through its cysteine-rich domain.Biochemical and biophysical research communications · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaphase is promoted by the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) only when all the chromosomes have achieved bipolar attachment to the mitotic spindles. Unattached kinetochores or the absence of tension between the paired kinetochores activates a surveillance mechanism termed the spindle-assembly checkpoint. A fundamental principle of the checkpoint is the activation of mitotic arrest deficient 2 (MAD2). MAD2 then forms a diffusible complex called mitotic checkpoint complex (designated as MAD2(MCC)) before it is recruited to APC/C (designated as MAD2(APC/C)). Large gaps in our knowledge remain on how MAD2 is inactivated after the checkpoint is satisfied. In this study, we have investigated the regulation of MAD2-containing complexes during mitotic progression. Using selective immunoprecipitation of checkpoint components and gel filtration chromatography, we found that MAD2(MCC) and MAD2(APC/C) were regulated very differently during mitotic exit. Temporally, MAD2(MCC) was broken down ahead of MAD2(APC/C). The inactivation of the two complexes also displayed different requirements of proteolysis; although APC/C and proteasome activities were dispensable for MAD2(MCC) inactivation, they are required for MAD2(APC/C) inactivation. In fact, the degradation of CDC20 is inextricably linked to the breakdown of MAD2(APC/C). These data extended our understanding of the checkpoint complexes during checkpoint silencing.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.