ArticleThe Journal of cell biology2022
Shared and specific functions of Arfs 1-5 at the Golgi revealed by systematic knockouts.
Article in The Journal of cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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
20 citing papers in PubMed, 35 citations in OpenAlex.
- Cytohesin-2 is essential for the perinatal development of mice and regulates Golgi volume.Life science alliance · 2026Article
- ARF GTPases Function at the Golgi.Sub-cellular biochemistry · 2026Review
- Arfs on the Golgi: four conductors, one orchestra.Frontiers in molecular biosciences · 2025Review
- Arf1-dependent LRBA recruitment to Rab4 endosomes is required for endolysosome homeostasis.The Journal of cell biology · 2024Article
- Membrane trafficking alterations in breast cancer progression.Frontiers in cell and developmental biology · 2024Review
- Enhanced SREBP2-driven cholesterol biosynthesis by PKCλ/ι deficiency in intestinal epithelial cells promotes aggressive serrated tumorigenesis.Nature communications · 2023Article
- The Arf-GAP Age2 localizes to the late-Golgi via a conserved amphipathic helix.Molecular biology of the cell · 2023Article
- ARF1 prevents aberrant type I interferon induction by regulating STING activation and recycling.Nature communications · 2023Article
- The development of resistance to an inhibitor of a cellular protein reveals a critical interaction between the enterovirus protein 2C and a small GTPase Arf1.PLoS pathogens · 2023Article
- The ARF GTPase regulatory network in collective invasion and metastasis.Biochemical Society transactions · 2023Review
- FTD/ALS Type 7-Associated Thr104Asn Mutation of CHMP2B Blunts Neuronal Process Elongation, and Is Recovered by Knockdown of Arf4, the Golgi Stress Regulator.Neurology international · 2023Article
- Arf1 coordinates fatty acid metabolism and mitochondrial homeostasis.Nature cell biology · 2023Article
- The Arf-GAP Age2 localizes to the late-Golgi via a conserved amphipathic helix.bioRxiv : the preprint server for biology · 2023Article
- STED imaging of endogenously tagged ARF GTPases reveals their distinct nanoscale localizations.The Journal of cell biology · 2023Article
- The Arf family GTPases: Regulation of vesicle biogenesis and beyond.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Review
- A neurodevelopmental disorder associated with an activating de novo missense variant in ARF1.Human molecular genetics · 2023Article
- Dysregulated proteostasis network in neuronal diseases.Frontiers in cell and developmental biology · 2023Review
- Dominant ARF3 variants disrupt Golgi integrity and cause a neurodevelopmental disorder recapitulated in zebrafish.Nature communications · 2022Article
- A CRISPR/Cas9-mediated screen identifies determinants of early plasma cell differentiation.Frontiers in immunology · 2022Article
- A general role for TANGO1, encoded by MIA3, in secretory pathway organization and function.Journal of cell science · 2021Article
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
ADP-ribosylation factors (Arfs) are small GTPases regulating membrane traffic in the secretory pathway. They are closely related and appear to have overlapping functions, regulators, and effectors. The functional specificity of individual Arfs and the extent of redundancy are still largely unknown. We addressed these questions by CRISPR/Cas9-mediated genomic deletion of the human class I (Arf1/3) and class II (Arf4/5) Arfs, either individually or in combination. Most knockout cell lines were viable with slight growth defects only when lacking Arf1 or Arf4. However, Arf1+4 and Arf4+5 could not be deleted simultaneously. Class I Arfs are nonessential, and Arf4 alone is sufficient for viability. Upon Arf1 deletion, the Golgi was enlarged, and recruitment of vesicle coats decreased, confirming a major role of Arf1 in vesicle formation at the Golgi. Knockout of Arf4 caused secretion of ER-resident proteins, indicating specific defects in coatomer-dependent ER protein retrieval by KDEL receptors. The knockout cell lines will be useful tools to study other Arf-dependent processes.
Indexed as
Identifiers
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.