ArticleThe Journal of cell biology2002
Assembly and function of AP-3 complexes in cells expressing mutant subunits.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
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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.
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Who cites it
71 citing papers in PubMed, 157 citations in OpenAlex.
- Structural mechanisms of cargo adaptors in membrane trafficking.Current opinion in cell biology · 2026Review
- 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
- Disordered hinge regions of the AP-3 adaptor complex promote vesicle budding from the late Golgi in yeast.Journal of cell science · 2024Article
- Adaptor protein complex interaction map in Arabidopsis identifies P34 as a common stability regulator.Nature plants · 2023Article
- An AP-3-dependent pathway directs phagosome fusion with Rab8 and Rab11 vesicles involved in TLR2 signaling.Traffic (Copenhagen, Denmark) · 2022Article
- Amyloid-like aggregating proteins cause lysosomal defects in neurons via gain-of-function toxicity.Life science alliance · 2022Article
- Role of adaptin protein complexes in intracellular trafficking and their impact on diseases.Bioengineered · 2021Article
- Wbox2: A clathrin terminal domain-derived peptide inhibitor of clathrin-mediated endocytosis.The Journal of cell biology · 2020Article
- Coatopathies: Genetic Disorders of Protein Coats.Annual review of cell and developmental biology · 2019Review
- Defective AP-3-dependent VAMP8 trafficking impairs Weibel-Palade body exocytosis in Hermansky-Pudlak Syndrome type 2 blood outgrowth endothelial cells.Haematologica · 2019Article
- The road to lysosome-related organelles: Insights from Hermansky-Pudlak syndrome and other rare diseases.Traffic (Copenhagen, Denmark) · 2019Review
- Neuronal functions of adaptor complexes involved in protein sorting.Current opinion in neurobiology · 2018Review
- Gene-edited MLE-15 Cells as a Model for the Hermansky-Pudlak Syndromes.American journal of respiratory cell and molecular biology · 2018Article
- Article
- New tools for "hot-wiring" clathrin-mediated endocytosis with temporal and spatial precision.The Journal of cell biology · 2017Article
- Contribution of the clathrin adaptor AP-1 subunit µ1 to acidic cluster protein sorting.The Journal of cell biology · 2017Article
- Article
- Upregulation of μ3A Drives Homeostatic Plasticity by Rerouting AMPAR into the Recycling Endosomal Pathway.Cell reports · 2016Article
- Article
- Loss of AP-5 results in accumulation of aberrant endolysosomes: defining a new type of lysosomal storage disease.Human molecular genetics · 2015Article
11 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
4 authors at 1 institution in 1 country.
Funding
Abstract
The mouse mutants mocha and pearl are deficient in the AP-3 delta and beta3A subunits, respectively. We have used cells from these mice to investigate both the assembly of AP-3 complexes and AP-3 function. In mocha cells, the beta3 and mu3 subunits coassemble into a heterodimer, whereas the sigma3 subunit remains monomeric. In pearl cells, the delta and sigma3 subunits coassemble into a heterodimer, whereas mu3 gets destroyed. The yeast two hybrid system was used to confirm these interactions, and also to demonstrate that the A (ubiquitous) and B (neuronal-specific) isoforms of beta3 and mu3 can interact with each other. Pearl cell lines were generated that express beta3A, beta3B, a beta3Abeta2 chimera, two beta3A deletion mutants, and a beta3A point mutant lacking a functional clathrin binding site. All six constructs assembled into complexes and were recruited onto membranes. However, only beta3A, beta3B, and the point mutant gave full functional rescue, as assayed by LAMP-1 sorting. The beta3Abeta2 chimera and the beta3A short deletion mutant gave partial functional rescue, whereas the beta3A truncation mutant gave no functional rescue. These results indicate that the hinge and/or ear domains of beta3 are important for function, but the clathrin binding site is not needed.
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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.