Evidence map›Paper›PMID 26551564›Full record

ArticleeLife2015

A G-protein activation cascade from Arl13B to Arl3 and implications for ciliary targeting of lipidated proteins.

Katja Gotthardt, Mandy Lokaj, Carolin Koerner, Nathalie Falk, Andreas Gießl, Alfred Wittinghofer

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
7.1field-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

97 citing papers in PubMed, 155 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. A Novel HeterozygousInternational journal of molecular sciences · 2026
    Article
  5. Molecular basis for the activation of outer dynein arms in cilia.Nature structural & molecular biology · 2025
    Article
  6. Ciliary ARL13B Is Essential for Vision and Morphogenesis of Cone Outer Segments.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Phosphoinositides in New Spaces.Cold Spring Harbor perspectives in biology · 2023
    Review
  18. Review
  19. RABL2 promotes the outward transition zone passage of signaling proteins in cilia via ARL3.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  20. Article

37 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

6 authors at 2 institutions in 1 country.

Katja GotthardtStructural Biology Group, Max Planck Institute of Molecular Physiology, Dortmund, Germany.
Mandy LokajStructural Biology Group, Max Planck Institute of Molecular Physiology, Dortmund, Germany.
Carolin KoernerStructural Biology Group, Max Planck Institute of Molecular Physiology, Dortmund, Germany.
Nathalie FalkDepartment of Biology, Animal Physiology, University of Erlangen-Nuremberg, Erlangen, Germany.
Andreas GießlDepartment of Biology, Animal Physiology, University of Erlangen-Nuremberg, Erlangen, Germany.
Alfred WittinghoferStructural Biology Group, Max Planck Institute of Molecular Physiology, Dortmund, Germany.
Max Planck Institute of Molecular Physiology · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small G-proteins of the ADP-ribosylation-factor-like (Arl) subfamily have been shown to be crucial to ciliogenesis and cilia maintenance. Active Arl3 is involved in targeting and releasing lipidated cargo proteins from their carriers PDE6δ and UNC119a/b to the cilium. However, the guanine nucleotide exchange factor (GEF) which activates Arl3 is unknown. Here we show that the ciliary G-protein Arl13B mutated in Joubert syndrome is the GEF for Arl3, and its function is conserved in evolution. The GEF activity of Arl13B is mediated by the G-domain plus an additional C-terminal helix. The switch regions of Arl13B are involved in the interaction with Arl3. Overexpression of Arl13B in mammalian cell lines leads to an increased Arl3·GTP level, whereas Arl13B Joubert-Syndrome patient mutations impair GEF activity and thus Arl3 activation. We anticipate that through Arl13B's exclusive ciliary localization, Arl3 activation is spatially restricted and thereby an Arl3·GTP compartment generated where ciliary cargo is specifically released.

Indexed as

ADP-Ribosylation FactorsAnimalsCiliaGuanine Nucleotide Exchange FactorsLipoproteinsMiceProtein BindingProtein Interaction MappingProtein TransportADP-Ribosylation FactorsArl13b protein, mouseArl3 protein, mouseGuanine Nucleotide Exchange FactorsLipoproteinsArf-like proteinsbiochemistrybiophysicsChlamydomonas reinhardtiiciliumG-proteinGuanine nucleotide exchange factorhumanmouseprotein traffickingstructural biology

Identifiers

PMID26551564
PMCPMC4868535
OpenAlexW2126210676

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.