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Syntenin-knock out reduces exosome turnover and viral transduction.

Rudra KashyapMarielle BalzanoBenoit LechatKathleen LambaertsAntonio Luis Egea-JimenezFrédérique LemboJoanna FaresSofie MeeussenSebastian KüglerAnton RoebroekGuido DavidPascale Zimmermann
Published in: Scientific reports (2021)
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.
Keyphrases
  • induced apoptosis
  • cell cycle arrest
  • cell surface
  • sars cov
  • type diabetes
  • metabolic syndrome
  • endoplasmic reticulum stress
  • adipose tissue
  • small molecule
  • transcription factor
  • body composition