Evidence map›Paper›PMID 21725319›Full record

ArticleNature cell biology2011

A SNX3-dependent retromer pathway mediates retrograde transport of the Wnt sorting receptor Wntless and is required for Wnt secretion.

Martin Harterink, Fillip Port, Magdalena J Lorenowicz, Ian J McGough, Marie Silhankova, Marco C Betist, Jan R T van Weering, Roy G H P van Heesbeen, Teije C Middelkoop, Konrad Basler and 2 more

Abstract read
In one paragraph

Article in Nature cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers.

0numbers the graph read from it
0cells of the map it votes in
208citing papers in PubMed
–field-weighted citation impact
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

208 citing papers in PubMed.

  1. Review
  2. SNX3 exacerbates hepatic fibrosis by amplifying TGF-Acta pharmaceutica Sinica. B · 2026
    Article
  3. Article
  4. Cargo-Adaptor Cooperation Programs Retromer Coat Architecture.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
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  10. Article
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  12. Identification of a VPS29 isoform with restricted association to Retriever and Retromer accessory proteins through autoinhibition.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Review
  14. Review
  15. Article
  16. Article
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  18. Article
  19. Article
  20. Article

148 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Martin HarterinkHubrecht Institute, Royal Academy of Arts and Sciences and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.
Fillip Port *Institute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.
Magdalena J Lorenowicz *Hubrecht Institute, Royal Academy of Arts and Sciences and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.
Ian J McGough *Henry Wellcome Integrated Signaling Laboratories, Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom.
Marie SilhankovaHubrecht Institute, Royal Academy of Arts and Sciences and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.
Marco C BetistHubrecht Institute, Royal Academy of Arts and Sciences and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.
Jan R T van WeeringHenry Wellcome Integrated Signaling Laboratories, Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom.
Roy G H P van HeesbeenHubrecht Institute, Royal Academy of Arts and Sciences and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.
Teije C MiddelkoopHubrecht Institute, Royal Academy of Arts and Sciences and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.
Konrad BaslerInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.
Peter J CullenHenry Wellcome Integrated Signaling Laboratories, Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom.
Hendrik C KorswagenHubrecht Institute, Royal Academy of Arts and Sciences and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT, Utrecht, The Netherlands.

Funding

Wellcome Trust 085743Wellcome Trust 086777/Z/08/ZWellcome Trust 089928Wellcome Trust 089928/Z/09/Z
6 · The paper itself

Abstract

Wnt proteins are lipid-modified glycoproteins that play a central role in development, adult tissue homeostasis and disease. Secretion of Wnt proteins is mediated by the Wnt-binding protein Wntless (Wls), which transports Wnt from the Golgi network to the cell surface for release. It has recently been shown that recycling of Wls through a retromer-dependent endosome-to-Golgi trafficking pathway is required for efficient Wnt secretion, but the mechanism of this retrograde transport pathway is poorly understood. Here, we report that Wls recycling is mediated through a retromer pathway that is independent of the retromer sorting nexins SNX1-SNX2 and SNX5-SNX6. We have found that the unrelated sorting nexin, SNX3, has an evolutionarily conserved function in Wls recycling and Wnt secretion and show that SNX3 interacts directly with the cargo-selective subcomplex of the retromer to sort Wls into a morphologically distinct retrieval pathway. These results demonstrate that SNX3 is part of an alternative retromer pathway that functionally separates the retrograde transport of Wls from other retromer cargo.

Indexed as

AnimalsAnimals, Genetically ModifiedBiological Transport, ActiveCaenorhabditis elegansDrosophilaEndosomesHeLa CellsHumansIntracellular Signaling Peptides and ProteinsModels, BiologicalRNA InterferenceSignal TransductionSorting Nexinstrans-Golgi NetworkWnt ProteinsIntracellular Signaling Peptides and ProteinsSNX3 protein, humanSorting NexinsWnt Proteins

Identifiers

PMID21725319
PMCPMC4052212

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Registered trials

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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.