ArticleThe EMBO journal2022
Defining the proximal interaction networks of Arf GTPases reveals a mechanism for the regulation of PLD1 and PI4KB.
Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 23 citations in OpenAlex.
- ARMH3 acts as a central scaffold at the Golgi/TGN through interactions with Arl5, GBF1, and PI4KB.The Journal of biological chemistry · 2026Article
- Architecture of clathrin-independent AP3:ARF1-coated carriers.Science advances · 2026Article
- Novel Insight into the Therapeutic Targets for Spinal Degenerative Diseases Gained by a Post-Genome-Wide Association Study.International journal of medical sciences · 2026Article
- ARF GTPases Function at the Golgi.Sub-cellular biochemistry · 2026Review
- A proximity map of RAB GTPases delineates roles for RAB14 in EARP complex and UHRF1BP1 endosomal recruitments.Communications biology · 2025Article
- Unfolding ARF and ARL GTPases: from biophysics to systems-level insights.Frontiers in molecular biosciences · 2025Review
- Arfs on the Golgi: four conductors, one orchestra.Frontiers in molecular biosciences · 2025Review
- ARF: the most misunderstood GTPase I ever knew - why study ARF GAPs.Frontiers in molecular biosciences · 2025Review
- Unlocking TRPM7 interactions: A database-driven quest.Computational and structural biotechnology journal · 2025Review
- ARMH3 is an ARL5 effector that promotes PI4KB-catalyzed PI4P synthesis at the trans-Golgi network.Nature communications · 2024Article
- Mapping the global interactome of the ARF family reveals spatial organization in cellular signaling pathways.Journal of cell science · 2024Article
- Axonal transport of autophagosomes is regulated by dynein activators JIP3/JIP4 and ARF/RAB GTPases.The Journal of cell biology · 2023Article
- The ARF GTPase regulatory network in collective invasion and metastasis.Biochemical Society transactions · 2023Review
- The Arf family GTPases: Regulation of vesicle biogenesis and beyond.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Review
- RUFY1 binds Arl8b and mediates endosome-to-TGN CI-M6PR retrieval for cargo sorting to lysosomes.The Journal of cell biology · 2023Article
- ARFs get the BioID treatment: what have we been missing?The EMBO journal · 2022Article
- Defining the proximal interaction networks of Arf GTPases reveals a mechanism for the regulation of PLD1 and PI4KB.The EMBO journal · 2022Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The Arf GTPase family is involved in a wide range of cellular regulation including membrane trafficking and organelle-structure assembly. Here, we have generated a proximity interaction network for the Arf family using the miniTurboID approach combined with TMT-based quantitative mass spectrometry. Our interactome confirmed known interactions and identified many novel interactors that provide leads for defining Arf pathway cell biological functions. We explored the unexpected finding that phospholipase D1 (PLD1) preferentially interacts with two closely related but poorly studied Arf family GTPases, ARL11 and ARL14, showing that PLD1 is activated by ARL11/14 and may recruit these GTPases to membrane vesicles, and that PLD1 and ARL11 collaborate to promote macrophage phagocytosis. Moreover, ARL5A and ARL5B were found to interact with and recruit phosphatidylinositol 4-kinase beta (PI4KB) at trans-Golgi, thus promoting PI4KB's function in PI4P synthesis and protein secretion.
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What Socratic 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 Socratic graph.