Evidence map›Paper›PMID 26659664›Full record

ArticleJournal of cell science2016

Activation of the IGF1 pathway mediates changes in cellular contractility and motility in single-suture craniosynostosis.

Zeinab Al-Rekabi, Marsha M Wheeler, Andrea Leonard, Adriane M Fura, Ilsa Juhlin, Christopher Frazar, Joshua D Smith, Sarah S Park, Jennifer A Gustafson, Christine M Clarke and 2 more

Abstract read
In one paragraph

Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Cell Mechanics of Craniosynostosis.ACS biomaterials science & engineering · 2017
    Article
  13. Genetic advances in craniosynostosis.American journal of medical genetics. Part A · 2017
    Review
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

12 authors at 2 institutions in 1 country.

Zeinab Al-RekabiDepartment of Mechanical Engineering, University of Washington, Seattle, WA 98195, USA Seattle Children's Research Institute, Center for Developmental Biology and Regenerative Medicine, Seattle, WA 98101, USA.
Marsha M WheelerDepartment of Genome Sciences, University of Washington, Seattle, WA 98105, USA.
Andrea LeonardDepartment of Mechanical Engineering, University of Washington, Seattle, WA 98195, USA.
Adriane M FuraDepartment of Bioengineering, University of Washington, Seattle, WA 98105, USA.
Ilsa JuhlinDepartment of Mechanical Engineering, University of Washington, Seattle, WA 98195, USA.
Christopher FrazarDepartment of Genome Sciences, University of Washington, Seattle, WA 98105, USA.
Joshua D SmithDepartment of Genome Sciences, University of Washington, Seattle, WA 98105, USA.
Sarah S ParkSeattle Children's Research Institute, Center for Developmental Biology and Regenerative Medicine, Seattle, WA 98101, USA.
Jennifer A GustafsonSeattle Children's Research Institute, Center for Developmental Biology and Regenerative Medicine, Seattle, WA 98101, USA.
Christine M ClarkeSeattle Children's Research Institute, Center for Developmental Biology and Regenerative Medicine, Seattle, WA 98101, USA.
Michael L CunninghamSeattle Children's Research Institute, Center for Developmental Biology and Regenerative Medicine, Seattle, WA 98101, USA Division of Craniofacial Medicine and the Department of Pediatrics, University of Washington, Seattle, WA 98105, USA.
Nathan J SniadeckiDepartment of Mechanical Engineering, University of Washington, Seattle, WA 98195, USA Department of Bioengineering, University of Washington, Seattle, WA 98105, USA nsniadec@uw.edu.
University of Washington · USSeattle Children's Hospital · US

Funding

SINGLE SUTURE CRANIOSYNOSTOSIS: CANDIDATE GENE AND PATHWAY DISCOVERYR01DE018227 · NIDCR · UNIVERSITY OF WASHINGTON · PI CUNNINGHAM, MICHAEL L · 2008 to 2017
$5.6M
NIDCR NIH HHS R01 DE018227NIDCR NIH HHS R01DE018227
6 · The paper itself

Abstract

Insulin growth factor 1 (IGF1) is a major anabolic signal that is essential during skeletal development, cellular adhesion and migration. Recent transcriptomic studies have shown that there is an upregulation in IGF1 expression in calvarial osteoblasts derived from patients with single-suture craniosynostosis (SSC). Upregulation of the IGF1 signaling pathway is known to induce increased expression of a set of osteogenic markers that previously have been shown to be correlated with contractility and migration. Although the IGF1 signaling pathway has been implicated in SSC, a correlation between IGF1, contractility and migration has not yet been investigated. Here, we examined the effect of IGF1 activation in inducing cellular contractility and migration in SSC osteoblasts using micropost arrays and time-lapse microscopy. We observed that the contractile forces and migration speeds of SSC osteoblasts correlated with IGF1 expression. Moreover, both contractility and migration of SSC osteoblasts were directly affected by the interaction of IGF1 with IGF1 receptor (IGF1R). Our results suggest that IGF1 activity can provide valuable insight for phenotype-genotype correlation in SSC osteoblasts and might provide a target for therapeutic intervention.

Indexed as

Cell AdhesionCell MovementCells, CulturedHumansInsulin-Like Growth Factor IOsteoblastsReceptor, IGF Type 1Signal TransductionIGF1 protein, humanInsulin-Like Growth Factor IReceptor, IGF Type 1Calvarial osteoblastCell migrationIGF1IGF1RSingle-suture craniosynostosisTraction force

Identifiers

PMID26659664
PMCPMC4760302
OpenAlexW2229628500

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.