Evidence map›Paper›PMID 21152103›Full record

ArticlePloS one2010

The mitotic arrest deficient protein MAD2B interacts with the clathrin light chain A during mitosis.

Klaas Medendorp, Lilian Vreede, Jan J M van Groningen, Lisette Hetterschijt, Linda Brugmans, Patrick A M Jansen, Wilhelmina H van den Hurk, Diederik R H de Bruijn, Ad Geurts van Kessel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. Review
  6. REV7: Jack of many trades.Trends in cell biology · 2021
    Review
  7. Clathrin Light Chains: Not to Be Taken so Lightly.Frontiers in cell and developmental biology · 2021
    Review
  8. Genome-wide DNA copy number analysis and targeted transcriptional analysis of canine histiocytic malignancies identifies diagnostic signatures and highlights disruption of spindle assembly complex.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019
    Article
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  11. Review
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  14. Review
  15. Article
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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

9 authors at 2 institutions in 1 country.

Klaas MedendorpDepartment of Human Genetics, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands.
Lilian Vreede
Jan J M van Groningen
Lisette Hetterschijt
Linda Brugmans
Patrick A M Jansen
Wilhelmina H van den Hurk
Diederik R H de Bruijn
Ad Geurts van Kessel
Radboud University Medical Center · NLRadboud University Nijmegen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlthough the mitotic arrest deficient protein MAD2B (MAD2L2) is thought to inhibit the anaphase promoting complex (APC) by binding to CDC20 and/or CDH1 (FZR1), its exact role in cell cycle control still remains to be established. METHODOLOGY/PRINCIPAL

findingsUsing a yeast two-hybrid interaction trap we identified the human clathrin light chain A (CLTA) as a novel MAD2B binding protein. A direct interaction was established in mammalian cells via GST pull-down and endogenous co-immunoprecipitation during the G2/M phase of the cell cycle. Through subsequent confocal laser scanning microscopy we found that MAD2B and CLTA co-localize at the mitotic spindle. Clathrin forms a trimeric structure, i.e., the clathrin triskelion, consisting of three heavy chains (CLTC), each with an associated light chain. This clathrin structure has previously been shown to be required for the function of the mitotic spindle through stabilization of kinetochore fibers. Upon siRNA-mediated MAD2B depletion, we found that CLTA was no longer concentrated at the mitotic spindle but, instead, diffusely distributed throughout the cell. In addition, we found a marked increase in the percentage of misaligned chromosomes. CONCLUSIONS/SIGNIFICANCE: Previously, we identified MAD2B as an interactor of the renal cell carcinoma (RCC)-associated protein PRCC. In addition, we found that fusion of PRCC with the transcription factor TFE3 in t(X;1)(p11;q21)-positive RCCs results in an impairment of this interaction and a concomitant failure to shuttle MAD2B to the nucleus. Our current data show that MAD2B interacts with CLTA during the G2/M phase of the cell cycle and that depletion of MAD2B leads to a marked increase in the percentage of misaligned chromosomes and a redistribution of CLTA during mitosis.

Indexed as

MitosisBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBlotting, WesternCell Cycle ProteinsCell Line, TumorClathrin Light ChainsG2 PhaseHEK293 CellsHumansImmunoprecipitationLuminescent ProteinsMad2 ProteinsMicroscopy, ConfocalNeoplasm ProteinsProtein BindingProteinsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell Cycle ProteinsClathrin Light ChainsLuminescent ProteinsMAD2L2 protein, humanMad2 ProteinsNeoplasm ProteinsPRCC protein, humanProteinsRecombinant Fusion ProteinsTFE3 protein, human

Identifiers

PMID21152103
PMCPMC2994903
OpenAlexW2059773530

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.