Evidence map›Paper›PMID 26963749›Full record

ArticleCell adhesion & migration2016

The ciliary GTPase Arl13b regulates cell migration and cell cycle progression.

Michal Pruski, Ann Rajnicek, Zhifu Yang, Hannah Clancy, Yu-Qiang Ding, Colin D McCaig, Bing Lang

Open access · goldAbstract read
In one paragraph

Article in Cell adhesion & migration, 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
2.7field-weighted citation impact, top 10% 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, 22 citations in OpenAlex.

  1. Review
  2. Neuronal guidance behaviours: the primary cilium perspective.Frontiers in cell and developmental biology · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. ARL13B, a Joubert Syndrome-Associated Protein, Is Critical for Retinogenesis and Elaboration of Mouse Photoreceptor Outer Segments.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  10. Review
  11. Article
  12. Article
  13. 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

7 authors at 3 institutions in 2 countries.

Michal Pruskia Key Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, and Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine , Shanghai , China.
Ann Rajnicekb School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, University of Aberdeen, Foresterhill , Aberdeen , Scotland , UK.
Zhifu Yangc Department of Pharmacy , Xijing Hospital, Fourth Military Medical University , Xi'an , Shaanxi , China.
Hannah Clancyb School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, University of Aberdeen, Foresterhill , Aberdeen , Scotland , UK.
Yu-Qiang Dinga Key Laboratory of Arrhythmias, Ministry of Education of China, East Hospital, and Department of Anatomy and Neurobiology, Collaborative Innovation Center for Brain Science, Tongji University School of Medicine , Shanghai , China.
Colin D McCaigb School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, University of Aberdeen, Foresterhill , Aberdeen , Scotland , UK.
Bing Langb School of Medicine, Medical Sciences and Nutrition, Institute of Medical Sciences, University of Aberdeen, Foresterhill , Aberdeen , Scotland , UK.
University of Aberdeen · GBTongji University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The GTPase ARL13B is localized to primary cilia; small cellular protrusions that act as antennae. Its defective ARL13B hennin (HNN) variant is linked causally with Joubert Syndrome, a developmental ciliopathy attributed to poor sensing of extracellular chemical gradients. We tested the hypothesis that impaired detection of extracellular voltage gradients also contributes to the HNN phenotype. In vitro, extracellular electric fields stimulated migration of wild type (WT) and HNN fibroblasts toward the cathode but the field only increased the migration speed of WT cells. Cilia on WT cells did not align to the field vector. HNN cells divided more slowly than WT cells, arresting at the G2/M phase. Mechanistically, HNN cells had reduced phospho-ERK1/2 signaling and elevated levels of Suppressor of Fused protein. These suggest that cells may not be able to read extracellular chemical cues appropriately, resulting in deficits in cell migration and proliferation. Finally, an increase in tubulin stabilization (more detyrosinated tubulin) confirmed the general stagnation of HNN cells, which may further contribute to slower migration and cell cycle progression. We conclude that Arl13b dysfunction resulted in HNN cell stagnation due to poor growth factor signaling and impaired detection of extracellular electrical gradients, and that the role of Arl13b in cell proliferation may be understated.

Indexed as

Cell CycleCell MovementADP-Ribosylation FactorsAnimalsCell CountCell ProliferationCiliaElectricityElectrodesExtracellular Signal-Regulated MAP KinasesG2 PhaseImmunohistochemistryMiceMicrotubulesMitosisModels, BiologicalADP-Ribosylation FactorsArl13b protein, mouseExtracellular Signal-Regulated MAP KinasesRepressor ProteinsSufu protein, mouseTubulinArl13bcell cycleciliopathiesHNNmigrationprimary cilium

Identifiers

PMID26963749
PMCPMC4986708
OpenAlexW2293542996

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.