ArticleJournal of cell science2013
Expression of OA1 limits the fusion of a subset of MVBs with lysosomes - a mechanism potentially involved in the initial biogenesis of melanosomes.
Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 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
24 citing papers in PubMed, 29 citations in OpenAlex.
- Dysregulated Polarized Secretion of Small Extracellular Vesicles in the Retinal Pigment Epithelium: Mechanisms and Pathological Roles in Age-Related Macular Degeneration.Journal of inflammation research · 2026Review
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- Genetics of Skin, Hair, and Eye Color in Human Pigmentation Disorders.Annals of human genetics · 2025Review
- Loss of REP-1 in retinal pigment epithelial cells leads to impaired phagosome processing and altered lysosomal pathway function.Molecular biology of the cell · 2025Article
- Specialised features of melanosomes in health and disease in the retinal pigment epithelium.Frontiers in cell and developmental biology · 2025Review
- G protein-coupled receptors: a gateway to targeting oncogenic EVs?Extracellular vesicles and circulating nucleic acids · 2024Review
- Impaired Lysosome Reformation in Chloroquine-Treated Retinal Pigment Epithelial Cells.Investigative ophthalmology & visual science · 2023Article
- A Comprehensive Review of Mammalian Pigmentation: Paving the Way for Innovative Hair Colour-Changing Cosmetics.Biology · 2023Review
- Inflammatory response: The target for treating hyperpigmentation during the repair of a burn wound.Frontiers in immunology · 2023Review
- Gold Particle Analyser: Detection and quantitative assessment of electron microscopy gold probes.PloS one · 2023Article
- The CACNA1A Mutant Disrupts Lysosome Calcium Homeostasis in Cerebellar Neurons and the Resulting Endo-Lysosomal Fusion Defect Can be Improved by Calcium Modulation.Neurochemical research · 2022Article
- Melanosome Biogenesis in the Pigmentation of Mammalian Skin.Integrative and comparative biology · 2021Review
- Nanoplasmonic Sensor Approaches for Sensitive Detection of Disease-Associated Exosomes.ACS applied bio materials · 2021Review
- Evidence for Protein-Protein Interaction between Dopamine Receptors and the G Protein-Coupled Receptor 143.International journal of molecular sciences · 2021Article
- Review
- Novel genetic variants ofAmerican journal of cancer research · 2020Article
- Identification of Novel G Protein-Coupled Receptor 143 Ligands as Pharmacologic Tools for Investigating X-Linked Ocular Albinism.Investigative ophthalmology & visual science · 2017Article
- Interaction between G Protein-Coupled Receptor 143 and Tyrosinase: Implications for Understanding Ocular Albinism Type 1.The Journal of investigative dermatology · 2017Article
- Mechanisms Associated with Activation of Intracellular Metabotropic Glutamate Receptor, mGluR5.Neurochemical research · 2017Article
- Ocular Albinism Type 1 Regulates Melanogenesis in Mouse Melanocytes.International journal of molecular sciences · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
Abstract
Multivesicular endosomes/bodies (MVBs) deliver proteins, such as activated EGF receptor (EGFR), to the lysosome for degradation, and, in pigmented cells, MVBs containing PMEL are an initial stage in melanosome biogenesis. The mechanisms regulating numbers and fate of different populations of MVB are unclear. Here, we focus on the role of the G-protein-coupled receptor OA1 (also known as GPR143), which is expressed exclusively in pigmented cells and mutations in which cause the most common type of ocular albinism. When exogenously expressing PMEL, HeLa cells have been shown to form MVBs resembling early stage melanosomes. To focus on the role of OA1 in the initial stages of melanosome biogenesis we take advantage of the absence of the later stages of melanosome maturation in HeLa cells to determine whether OA1 activity can regulate MVB number and fate. Expression of wild-type but not OA1 mutants carrying inactivating mutations or deletions causes MVB numbers to increase. Whereas OA1 expression has no effect on delivery of EGFR-containing MVBs to the lysosome, it inhibits the lysosomal delivery of PMEL and PMEL-containing MVBs accumulate. We propose that OA1 activity delays delivery of PMEL-containing MVBs to the lysosome to allow time for melanin synthesis and commitment to melanosome biogenesis.
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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.