ArticleTraffic (Copenhagen, Denmark)2021
Genetically encoded multimode reporter of adaptor complex 3 traffic in budding yeast.
Article in Traffic (Copenhagen, Denmark), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Septins associate with AP-3 to support trafficking to the vacuole/lysosome in yeast.Molecular biology of the cell · 2026Article
- Septins associate with AP-3 to support trafficking to the vacuole/lysosome in yeast.bioRxiv : the preprint server for biology · 2026Article
- Disordered hinge regions of the AP-3 adaptor complex promote vesicle budding from the late Golgi in yeast.Journal of cell science · 2024Article
- Fast-evolving cofactors regulate the role of HEATR5 complexes in intra-Golgi trafficking.The Journal of cell biology · 2024Article
- Two functionally distinct HEATR5 protein complexes are defined by fast-evolving co-factors in yeast.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
AP-3 (adaptor complex 3) mediates traffic from the late Golgi or early endosomes to late endosomal compartments. In mammals, mutations in AP-3 cause Hermansky-Pudlak syndrome type 2, cyclic neutropenias, and a form of epileptic encephalopathy. In budding yeast, AP-3 carries cargo directly from the trans-Golgi to the lysosomal vacuole. Despite the pathway's importance and its discovery two decades ago, rapid screens and selections for AP-3 mutants have not been available. We now report GNSI, a synthetic, genetically encoded reporter that allows rapid plate-based assessment of AP-3 functional deficiency, using either chromogenic or growth phenotype readouts. This system identifies defects in both the formation and consumption of AP-3 carrier vesicles and is adaptable to high-throughput screening or selection in both plate array and liquid batch culture formats. Episomal and integrating plasmids encoding GNSI have been submitted to the Addgene repository.
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What OpenQuestion holds
Registered trials
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.