ArticleMolecular biology of the cell2019
Adaptor protein-3 complex is required for Vangl2 trafficking and planar cell polarity of the inner ear.
Article in Molecular biology of the cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Article
- Article
- A homozygous AP3D1 missense variant in patients with sensorineural hearing loss as the leading manifestation.Human genetics · 2023Article
- Article
- Vangl as a Master Scaffold for Wnt/Planar Cell Polarity Signaling in Development and Disease.Frontiers in cell and developmental biology · 2022Review
- Article
- Regulation of Wnt/PCP signaling through p97/VCP-KBTBD7-mediated Vangl ubiquitination and endoplasmic reticulum-associated degradation.Science advances · 2021Article
- AP-3 adaptor complex-mediated vesicle trafficking.Biophysics reports · 2021Article
- Molecular mechanisms mediating asymmetric subcellular localisation of the core planar polarity pathway proteins.Biochemical Society transactions · 2020Review
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Authors and funding
8 authors.
Funding
Abstract
Planar cell polarity (PCP) regulates coordinated cellular polarity among neighboring cells to establish a polarity axis parallel to the plane of the tissue. Disruption in PCP results in a range of developmental anomalies and diseases. A key feature of PCP is the polarized and asymmetric localization of several membrane PCP proteins, which is essential to establish the polarity axis to orient cells coordinately. However, the machinery that regulates the asymmetric partition of PCP proteins remains largely unknown. In the present study, we show Van gogh-like 2 (Vangl2) in early and recycling endosomes as made evident by colocalization with diverse endosomal Rab proteins. Vangl2 biochemically interacts with adaptor protein-3 complex (AP-3). Using short hairpin RNA knockdown, we found that Vangl2 subcellular localization was modified in AP-3-depleted cells. Moreover, Vangl2 membrane localization within the cochlea is greatly reduced in AP-3-deficient
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