Evidence map›Paper›PMID 16184168›Full record

ArticleNature cell biology2005

The focal adhesion scaffolding protein HEF1 regulates activation of the Aurora-A and Nek2 kinases at the centrosome.

Elena N Pugacheva, Erica A Golemis

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 1 pooled it
6.3field-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

136 citing papers in PubMed, 1 synthesis or guideline pooled it, 232 citations in OpenAlex.

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76 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

2 authors at 1 institution in 1 country.

Elena N PugachevaDivision of Basic Science, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA.
Erica A Golemis
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Dietmar J Kappes · 1985 to 2026
$138.8M
ROLES OF HEF1 IN CELL DIFFERENTIATION AND SURVIVALR01CA063366 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI GOLEMIS, ERICA A. · 1998 to 2013
$3.9M
CONTROL OF NORMAL AND ABNORMAL CELL GROWTHR29CA063366 · NCI · INSTITUTE FOR CANCER RESEARCH · PI GOLEMIS, ERICA A · 1994 to 1997
–
NCI NIH HHS CA-06927NCI NIH HHS CA63366NCI NIH HHS P30 CA006927NCI NIH HHS R01 CA063366
6 · The paper itself

Abstract

Although HEF1 has a well-defined role in integrin-dependent attachment signalling at focal adhesions, it relocalizes to the spindle asters at mitosis. We report here that overexpression of HEF1 causes an increase in centrosome numbers and multipolar spindles, resembling defects induced by manipulation of the mitotic regulatory kinase Aurora-A (AurA). We show that HEF1 associates with and controls activation of AurA. We also show that HEF1 depletion causes centrosomal splitting, mono-astral spindles and hyperactivation of Nek2, implying additional action earlier in the cell cycle. These results provide new insight into the role of an adhesion protein in coordination of cell attachment and division.

Indexed as

Adaptor Proteins, Signal TransducingAurora KinasesCell CycleCell Line, TumorCentrosomeEnzyme ActivationFocal AdhesionsHeLa CellsHumansNIMA-Related KinasesPhosphoproteinsProtein Serine-Threonine KinasesSpindle ApparatusAdaptor Proteins, Signal TransducingAurora KinasesNEDD9 protein, humanNEK2 protein, humanNIMA-Related KinasesPhosphoproteinsProtein Serine-Threonine Kinases

Identifiers

PMID16184168
PMCPMC2652766
OpenAlexW2093043664

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.