Evidence map›Paper›PMID 22037211›Full record

ArticleCell cycle (Georgetown, Tex.)2011

Closed MAD2 (C-MAD2) is selectively incorporated into the mitotic checkpoint complex (MCC).

Aaron R Tipton, Michael Tipton, Tim Yen, Song-Tao Liu

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. MAD1: Kinetochore Receptors and Catalytic Mechanisms.Frontiers in cell and developmental biology · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. The end of mitosis from a phosphatase perspective.Cell cycle (Georgetown, Tex.) · 2013
    Article
  19. 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

4 authors at 2 institutions in 1 country.

Aaron R TiptonDepartment of Biological Sciences, University of Toledo, Toledo, OH, USA.
Michael Tipton
Tim Yen
Song-Tao Liu
University of Toledo · USPhiladelphia University · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
KINETOCHORE STRUCTURE/FUNCTIONR01GM044762 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI YEN, TIMOTHY · 1992 to 2010
$2.4M
Mechanism of Mitotic Checkpoint in Mammalian CellsR01GM086877 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI YEN, TIMOTHY · 2008 to 2011
$1.6M
NCI NIH HHS CA06927NCI NIH HHS P30 CA006927NIGMS NIH HHS GM44762NIGMS NIH HHS GM86877NIGMS NIH HHS R01 GM044762NIGMS NIH HHS R01 GM086877
6 · The paper itself

Abstract

The mitotic checkpoint is a specialized signal transduction pathway that monitors kinetochore-microtubule attachment to achieve faithful chromosome segregation. MAD2 is an evolutionarily conserved mitotic checkpoint protein that exists in open (O) and closed (C) conformations. The increase of intracellular C-MAD2 level during mitosis, through O→C-MAD2 conversion as catalyzed by unattached kinetochores, is a critical signaling event for the mitotic checkpoint. However, it remains controversial whether MAD2 is an integral component of the effector of the mitotic checkpoint--the Mitotic Checkpoint Complex (MCC). We show here that endogenous human MCC is assembled by first forming a BUBR1:BUB3:CDC20 complex in G2 and then selectively incorporating C-MAD2 during mitosis. Nevertheless, MCC can be induced to form in G1/S cells by expressing a C-conformation locked MAD2 mutant, indicating intracellular level of C-MAD2 as a major limiting factor for MCC assembly. In addition, a recombinant MCC containing C-MAD2 exhibits effective inhibitory activity towards APC/C isolated from mitotic HeLa cells, while a recombinant BUBR1:BUB3:CDC20 ternary complex is ineffective at comparable concentrations despite association with APC/C. These results help establish a direct connection between a major signal transducer (C-MAD2) and the potent effector (MCC) of the mitotic checkpoint, and provide novel insights into protein-protein interactions during assembly of a functional MCC.

Indexed as

Calcium-Binding ProteinsCdc20 ProteinsCell Cycle ProteinsHeLa CellsHumansMad2 ProteinsMitosisM Phase Cell Cycle CheckpointsMultiprotein ComplexesPoly-ADP-Ribose Binding ProteinsProtein ConformationProtein Serine-Threonine KinasesRepressor ProteinsBUB1 protein, humanBub1 spindle checkpoint proteinBUB3 protein, humanCalcium-Binding ProteinsCDC20 protein, humanCdc20 ProteinsCell Cycle ProteinsMAD2L1 protein, humanMad2 ProteinsMultiprotein ComplexesPoly-ADP-Ribose Binding ProteinsProtein Serine-Threonine KinasesRepressor Proteins

Identifiers

PMID22037211
PMCPMC3266009
OpenAlexW2013066261

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.