Evidence map›Paper›PMID 9744883›Full record

ArticleThe Journal of cell biology1998

Active MAP kinase in mitosis: localization at kinetochores and association with the motor protein CENP-E.

M Zecevic, A D Catling, S T Eblen, L Renzi, J C Hittle, T J Yen, G J Gorbsky, M J Weber

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 217 citations in OpenAlex.

  1. Trial
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  8. Hyper-active RAS/MAPK introduces cancer-specific mitotic vulnerabilities.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Sensitivity toCancer research · 2017
    Article
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  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

23 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

M ZecevicDepartment of Microbiology and Cancer Center, University of Virginia, Health Sciences Center, Charlottesville, Virginia 22908, USA.
A D Catling
S T Eblen
L Renzi
J C Hittle
T J Yen
G J Gorbsky
M J Weber
Fox Chase Cancer Center · USUniversity of Virginia · US

Funding

CHROMOSOME MOVEMENT IN PROMETAPHASER01GM050412 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GORBSKY, GARY J. · 1994 to 2012
$4.5M
KINETOCHORE STRUCTURE/FUNCTIONR01GM044762 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI YEN, TIMOTHY · 1992 to 2010
$2.4M
SIGNAL TRANSDUCTION BY TYROSINE KINASESR01CA039076 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI WEBER, MICHAEL J · 1985 to 2001
$488k
P42/MAP KINASE: STRUCTURE, FUNCTION AND REGULATIONR01GM047332 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI WEBER, MICHAEL J · 1992 to 2000
$227k
SIGNAL TRANSMISSION BY THE SRC ONCOGENER37CA039076 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI WEBER, MICHAEL J · 1989 to 1996
–
NCI NIH HHS CA-39076NIGMS NIH HHS GM-47332NIGMS NIH HHS GM-50412NIGMS NIH HHS R01 GM044762NIGMS NIH HHS R01 GM050412
6 · The paper itself

Abstract

To investigate possible involvement of the mitogen-activated protein (MAP) kinases ERK1 and ERK2 (extracellular signal-regulated kinases) in somatic cell mitosis, we have used indirect immunofluorescence with a highly specific phospho-MAP kinase antibody and found that a portion of the active MAP kinase is localized at kinetochores, asters, and the midbody during mitosis. Although the aster labeling was constant from the time of nuclear envelope breakdown, the kinetochore labeling first appeared at early prometaphase, started to fade during chromosome congression, and then disappeared at midanaphase. At telophase, active MAP kinase localized at the midbody. Based on colocalization and the presence of a MAP kinase consensus phosphorylation site, we identified the kinetochore motor protein CENP-E as a candidate mitotic substrate for MAP kinase. CENP-E was phosphorylated in vitro by MAP kinase on sites that are known to regulate its interactions with microtubules and was found to associate in vivo preferentially with the active MAP kinase during mitosis. Therefore, the presence of active MAP kinase at specific mitotic structures and its interaction with CENP-E suggest that MAP kinase could play a role in mitosis at least in part by altering the ability of CENP-E to mediate interactions between chromosomes and microtubules.

Indexed as

Mitogen-Activated Protein KinasesMitosis3T3 CellsAnimalsCalcium-Calmodulin-Dependent Protein KinasesCell LineChromosomal Proteins, Non-HistoneChromosomesEnzyme ActivationHeLa CellsHumansKinetochoresMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationCalcium-Calmodulin-Dependent Protein Kinasescentromere protein EChromosomal Proteins, Non-HistoneMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinases

Identifiers

PMID9744883
PMCPMC2141767
OpenAlexW2080628130

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.