ArticlePLoS biology2018
Role of the AP-5 adaptor protein complex in late endosome-to-Golgi retrieval.
Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled 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.
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.
Who cites it
68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 127 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Assessing sub-cellular resolution in spatial proteomics experiments.Current opinion in chemical biology · 2019Pooled it
- Endosomes as central hubs of interorganellar communication and cellular homeostasis.Protein & cell · 2026Review
- Bi-allelic variants in AP5Z1 and AP5B1 lead to retinal degeneration.HGG advances · 2026Article
- MUDENG, a component of adaptor complex 5, mediates TRAIL- and TMZ-triggered apoptosis in glioblastoma (GBM) via multiple pathways.Apoptosis : an international journal on programmed cell death · 2026Article
- Review
- Article
- Structural basis for membrane remodeling by the AP5-SPG11-SPG15 complex.Nature structural & molecular biology · 2025Article
- Disruption of Retriever Function Impacts Retrograde Trafficking From Endosomes.Cell biology international · 2025Article
- AP5Z1 affects hepatocellular carcinoma growth and autophagy by regulating PTEN ubiquitination and modulating the PI3K/Akt/mTOR pathway.Journal of translational medicine · 2025Article
- Adaptor Protein Complexes in HIV-1 Pathogenesis: Mechanisms and Therapeutic Potential.Viruses · 2025Review
- Bi-allelic variants in three genes encoding distinct subunits of the vesicular AP-5 complex cause hereditary macular dystrophy.American journal of human genetics · 2025Article
- Inhibition of OSBP blocks retrograde trafficking by inducing partial Golgi degradation.Nature chemical biology · 2025Article
- Genome-wide identification of the adaptor protein complexes and its expression patterns analysis in foxtail millet (Setaria italica L.).BMC plant biology · 2025Article
- An updated Bioconductor workflow for correlation profiling subcellular proteomics.F1000Research · 2025Article
- Development and validation of a risk prediction model for diabetic kidney disease in patients with diabetic retinopathy.Frontiers in endocrinology · 2025Article
- Spatial proteomics: unveiling the multidimensional landscape of protein localization in human diseases.Proteome science · 2024Review
- When less is more - a fast TurboID knock-in approach for high-sensitivity endogenous interactome mapping.Journal of cell science · 2024Article
- A genetically-encoded fluorescence-based reporter to spatiotemporally investigate mannose-6-phosphate pathway.Molecular biology of the cell · 2024Article
- Maternal regulation of the vertebrate oocyte-to-embryo transition.PLoS genetics · 2024Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The AP-5 adaptor protein complex is presumed to function in membrane traffic, but so far nothing is known about its pathway or its cargo. We have used CRISPR-Cas9 to knock out the AP-5 ζ subunit gene, AP5Z1, in HeLa cells, and then analysed the phenotype by subcellular fractionation profiling and quantitative mass spectrometry. The retromer complex had an altered steady-state distribution in the knockout cells, and several Golgi proteins, including GOLIM4 and GOLM1, were depleted from vesicle-enriched fractions. Immunolocalisation showed that loss of AP-5 led to impaired retrieval of the cation-independent mannose 6-phosphate receptor (CIMPR), GOLIM4, and GOLM1 from endosomes back to the Golgi region. Knocking down the retromer complex exacerbated this phenotype. Both the CIMPR and sortilin interacted with the AP-5-associated protein SPG15 in pull-down assays, and we propose that sortilin may act as a link between Golgi proteins and the AP-5/SPG11/SPG15 complex. Together, our findings suggest that AP-5 functions in a novel sorting step out of late endosomes, acting as a backup pathway for retromer. This provides a mechanistic explanation for why mutations in AP-5/SPG11/SPG15 cause cells to accumulate aberrant endolysosomes, and highlights the role of endosome/lysosome dysfunction in the pathology of hereditary spastic paraplegia and other neurodegenerative disorders.
Indexed as
Identifiers
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.