ArticleJournal of cell science2021
BPIFB3 interacts with ARFGAP1 and TMED9 to regulate non-canonical autophagy and RNA virus infection.
Article in Journal of cell science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 11 citations in OpenAlex.
- ARFGAP1 serves as a critical host factor during E30 infection: QS11 inhibits viral pathogenesis in hFcRn-IFNARVirology journal · 2025Article
- Hydroxychloroquine's diverse targets: a new frontier in precision medicine.Frontiers in immunology · 2025Review
- TMED9: a potential therapeutic target and prognostic marker in glioma and its implications across pan-cancer contexts.Frontiers in immunology · 2025Article
- Article
- Prognostic value and anti-tumor immunity role ofTranslational cancer research · 2024Article
- A nasal cell atlas reveals heterogeneity of tuft cells and their role in directing olfactory stem cell proliferation.Science immunology · 2024Article
- Quantitative Proteomics Explore the Potential Targets and Action Mechanisms of Hydroxychloroquine.Molecules (Basel, Switzerland) · 2022Article
- The many hats of transmembrane emp24 domain protein TMED9 in secretory pathway homeostasis.Frontiers in cell and developmental biology · 2022Review
- High expression of transmembrane P24 trafficking protein 9 predicts poor prognosis in breast carcinoma.Bioengineered · 2021Article
- ER-Phagy and Microbial Infection.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Autophagy is a degradative cellular pathway that targets cytoplasmic contents and organelles for turnover by the lysosome. Various autophagy pathways play key roles in the clearance of viral infections, and many families of viruses have developed unique methods for avoiding degradation. Some positive-stranded RNA viruses, such as enteroviruses and flaviviruses, usurp the autophagic pathway to promote their own replication. We previously identified the endoplasmic reticulum (ER)-localized protein BPIFB3 as an important negative regulator of non-canonical autophagy that uniquely impacts the replication of enteroviruses and flaviviruses. Here, we find that many components of the canonical autophagy machinery are not required for BPIFB3 depletion-induced autophagy and identify the host factors that facilitate its role in the replication of enteroviruses and flaviviruses. Using proximity-dependent biotinylation (BioID) followed by mass spectrometry, we identify ARFGAP1 and TMED9 as two cellular components that interact with BPIFB3 to regulate autophagy and viral replication. Importantly, our data demonstrate that non-canonical autophagy in mammalian cells can be controlled outside of the traditional pathway regulators and define the role of two proteins in BPIFB3 depletion mediated non-canonical autophagy.
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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.