ArticleCommunications biology2026
Coro1a promotes the multivesicular body and plasma membrane fusion by facilitating PKM2-mediated SNAP-23 phosphorylation.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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Who cites it
1 citing paper in PubMed.
- Exosome-Mediated Systemic Signaling: Mechanisms, Disease Integration, and Translational Potential.Current issues in molecular biology · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
The release of exosomes involves the fusion of multivesicular bodies (MVBs) with the plasma membrane (PM), a process driven by the soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex. However, the specific SNARE complex mediating MVB-PM fusion and its regulatory mechanism remain unclear. Here, we show that Coronin-1a (Coro1a) increases extracellular vesicle (EV) biogenesis by promoting the assembly of the STX-12-SNAP-23-VAMP-7 SNARE complex independent of neddylation. Mechanistically, Coro1a activates pyruvate kinase M2 (PKM2) to enhance SNAP-23 phosphorylation, thereby driving the recruitment of STX-12 and VAMP-7. Consequently, Coro1a-induced EV biogenesis is abolished by PKM2 inhibition or SNAP-23 silencing. Furthermore, Coro1a levels are elevated in lung tumor tissues and correlate with poor patient survival, suggesting that Coro1a-mediated enhancement of EV production contributes to tumor progression. Our data demonstrate that Coro1a facilitates EV biogenesis by promoting SNARE complex assembly during MVB and PM fusion.
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