ArticleThe EMBO journal2014
Old dog, new tricks: Arf1 required for mitochondria homeostasis.
Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Divergent Role of ULK1 to Balance Mitochondrial Homeostasis and Bioenergetics in Ovarian Cancer Spheroids.Cancers · 2026Article
- Apolipoproteins L involvement in immunity.Journal of human immunity · 2026Review
- ARF1 prevents aberrant type I interferon induction by regulating STING activation and recycling.Nature communications · 2023Article
- The SNAP25 Interactome in Ventromedial Caudate in Schizophrenia Includes the Mitochondrial Protein ARF1.Neuroscience · 2019Article
- ER fatalities-The role of ER-mitochondrial contact sites in yeast life and death decisions.Mechanisms of ageing and development · 2017Review
- Article
- Altered Gene Expression in the Schistosome-Transmitting Snail Biomphalaria glabrata following Exposure to Niclosamide, the Active Ingredient in the Widely Used Molluscicide Bayluscide.PLoS neglected tropical diseases · 2015Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The small GTPase Arf1 that is classically required for the budding of COPI-coated vesicles from the Golgi membrane is now proposed to have novel and conserved roles in the morphological and functional maintenance of mitochondria: It functionally localizes to ER/mitochondria contact sites; it allows for the recruitment of a degradation machinery to mitochondria to remove toxic mitofusin/Fzo1 clusters; and it allows the extension of autophagy sequestration membranes needed for mitophagy to clear damaged mitochondria.
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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.