4.7 Article

Syntenin-knock out reduces exosome turnover and viral transduction

Journal

SCIENTIFIC REPORTS
Volume 11, Issue 1, Pages -

Publisher

NATURE RESEARCH
DOI: 10.1038/s41598-021-81697-4

Keywords

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Funding

  1. Concerted Actions Program of the KU Leuven [GOA/12/016]
  2. Belgian Foundation against cancer (STK) [FA/2014/294]
  3. French Foundation for Cancer Research (ARC) [PJA 20141201624]
  4. Institut National du Cancer (INCa) [2013-105]
  5. National Research Agency (ANR, Investissements d'Avenir, A*MIDEX project) [ANR-11-IDEX-0001-02]
  6. Fund for Scientific Research-Flanders (FWO) [G.0846.15]
  7. Ligue French Foundation for Cancer Research
  8. Ligue contre le Cancer (France)
  9. European Union's Horizon 2020 research and innovation program under the Marie Sklodowska-Curie Grant [747025]
  10. Marie Curie Actions (MSCA) [747025] Funding Source: Marie Curie Actions (MSCA)

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Syntenin plays a crucial role in exosomal transfers by directing endocytosed cargo to budding endosomal membranes and supporting viral/exosomal exchanges. It, along with heparan sulfate proteoglycans, is identified as a key component for macromolecular cargo internalization into cells.
Exosomal transfers represent an important mode of intercellular communication. Syntenin is a small scaffold protein that, when binding ALIX, can direct endocytosed syndecans and syndecan cargo to budding endosomal membranes, supporting the formation of intraluminal vesicles that compose the source of a major class of exosomes. Syntenin, however, can also support the recycling of these same components to the cell surface. Here, by studying mice and cells with syntenin-knock out, we identify syntenin as part of dedicated machinery that integrates both the production and the uptake of secreted vesicles, supporting viral/exosomal exchanges. This study significantly extends the emerging role of heparan sulfate proteoglycans and syntenin as key components for macromolecular cargo internalization into cells.

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