| First Author | Kashyap R | Year | 2021 |
| Journal | Sci Rep | Volume | 11 |
| Issue | 1 | Pages | 4083 |
| PubMed ID | 33602969 | Mgi Jnum | J:303742 |
| Mgi Id | MGI:6512744 | Doi | 10.1038/s41598-021-81697-4 |
| Citation | Kashyap R, et al. (2021) Syntenin-knock out reduces exosome turnover and viral transduction. Sci Rep 11(1):4083 |
| abstractText | 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. |
