ArticleNature communications2025
Autophagy-independent role of ATG9A vesicles as carriers for galectin-9 secretion.
Article in Nature communications, 2025. 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.
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Who cites it
7 citing papers in PubMed.
- The ER-Golgi intermediate compartment: a central hub integrating membrane trafficking and stress responses.EMBO reports · 2026Review
- Glycoprotein-induced phase separation drives unconventional secretion of galectin-3.Nature communications · 2026Article
- Mechanisms and therapeutic implications of galectins regulating Epstein-Barr virus infection.Virus research · 2026Review
- Review
- The role of galectins in modulating the tumor microenvironment and driving metastasis in skin cancers.Biological research · 2026Review
- Galectin-9 binding to HLA-DR in dendritic cells controls immune synapse formation and T cell proliferation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Beyond the Secretory Pathway: New Insights Into Protein Release.Traffic (Copenhagen, Denmark) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Galectins play vital roles in cellular processes such as adhesion, communication, and survival, yet the mechanisms underlying their unconventional secretion remain poorly understood. This study identifies ATG9A, a core autophagy protein, as a key regulator of galectin-9 secretion via a mechanism independent of classical autophagy, secretory autophagy, or the LC3-dependent extracellular vesicle loading and secretion pathway. ATG9A vesicles function as specialized carriers, with the N-terminus of ATG9A and both carbohydrate recognition domains of galectin-9 being critical for the process. TMED10 mediates the incorporation of galectin-9 into ATG9A vesicles, which then fuse with the plasma membrane via the STX13-SNAP23-VAMP3 SNARE complex. Furthermore, ATG9A regulates the secretion of other proteins, including galectin-4, galectin-8, and annexin A6, but not IL-1β, galectin-3, or FGF2. This mechanism is potentially conserved across other cell types, including monocytic cells, which underscores its broader significance in unconventional protein secretion.
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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.