Evidence map›Paper›PMID 9396744›Full record

ArticleThe Journal of cell biology1997

CENP-E function at kinetochores is essential for chromosome alignment.

B T Schaar, G K Chan, P Maddox, E D Salmon, T J Yen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

148 citing papers in PubMed, 326 citations in OpenAlex.

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  11. Molecular evolution of the mammalian kinetochore complex.bioRxiv : the preprint server for biology · 2024
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88 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

5 authors at 2 institutions in 1 country.

B T SchaarCell and Molecular Biology Graduate Group, University of Pennsylvania, Philadelphia, Pennsylvania 19103, USA.
G K Chan
P Maddox
E D Salmon
T J Yen
University of North Carolina at Chapel Hill · USFox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
MECHANISMS OF MITOTIC SPINDLE ASSEMBLY AND FUNCTIONR37GM024364 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SALMON, EDWARD D. · 2004 to 2013
$4.1M
MECHANISMS OF MITOTIC SPINDLE ASSEMBLY AND FUNCTIONR01GM024364 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOOM, KERRY S, SALMON, EDWARD D. · 1985 to 2018
$3.1M
KINETOCHORE STRUCTURE/FUNCTIONR01GM044762 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI YEN, TIMOTHY · 1992 to 2010
$2.4M
NCI NIH HHS CA06927NCI NIH HHS P30 CA006927NIGMS NIH HHS GM24364NIGMS NIH HHS GM44762NIGMS NIH HHS R01 GM024364NIGMS NIH HHS R01 GM044762NIGMS NIH HHS R37 GM024364
6 · The paper itself

Abstract

CENP-E is a kinesin-like protein that binds to kinetochores and may provide functions that are critical for normal chromosome motility during mitosis. To directly test the in vivo function of CENP-E, we microinjected affinity-purified antibodies to block the assembly of CENP-E onto kinetochores and then examined the behavior of these chromosomes. Chromosomes lacking CENP-E at their kinetochores consistently exhibited two types of defects that blocked their alignment at the spindle equator. Chromosomes positioned near a pole remained mono-oriented as they were unable to establish bipolar microtubule connections with the opposite pole. Chromosomes within the spindle established bipolar connections that supported oscillations and normal velocities of kinetochore movement between the poles, but these bipolar connections were defective because they failed to align the chromosomes into a metaphase plate. Overexpression of a mutant that lacked the amino-terminal 803 amino acids of CENP-E was found to saturate limiting binding sites on kinetochores and competitively blocked endogenous CENP-E from assembling onto kinetochores. Chromosomes saturated with the truncated CENP-E mutant were never found to be aligned but accumulated at the poles or were strewn within the spindle as was the case when cells were microinjected with CENP-E antibodies. As the motor domain was contained within the portion of CENP-E that was deleted, the chromosomal defect is likely attributed to the loss of motor function. The combined data show that CENP-E provides kinetochore functions that are essential for monopolar chromosomes to establish bipolar connections and for chromosomes with connections to both spindle poles to align at the spindle equator. Both of these events rely on activities that are provided by CENP-E's motor domain.

Indexed as

AnimalsAntibodiesCell LineChromosomal Proteins, Non-HistoneChromosomesGreen Fluorescent ProteinsHeLa CellsHumansKineticsKinetochoresLuminescent ProteinsMitosisModels, BiologicalMutagenesisRabbitsRecombinant Fusion ProteinsAntibodiescentromere protein EChromosomal Proteins, Non-HistoneGreen Fluorescent ProteinsLuminescent ProteinsRecombinant Fusion Proteins

Identifiers

PMID9396744
PMCPMC2132614
OpenAlexW2132680465

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.