The double knockdown of SNX17 and SNX27 results in a striking reduction of papillomavirus 16 infection due to interruption of their binding to the L2 viral protein.
SNX17 plays a role in the maintenance of normal surface levels of activating receptors and integrins to permit optimum T cell activation at the immune synapse.
Data indicate that the major binding site for binding of sorting nexin 17 (SNX17) is confined to the NPXF2 motif in cytoplasmic adaptor protein Krev interaction trapped 1 (KRIT1).
The authors demonstrate that SNX17 is essential for infection with all papillomavirus types analyzed indicating an evolutionarily highly conserved virus entry mechanism.
Snx 17 binds to a motif in the low-density lipoprotein (LDL) receptor-related protein (LRP) tail distinct from the endocytosis signals and promotes LRP sorting to the recycling pathway in the early endosomes.
expression level of SNX17 may regulate the lysosomal degradation at least for P-selectin by suppressing its entry into the inner vesicles of the multi-vesicular bodies (MVBs)
We'd like to inform you that we have updated our Privacy Notice to comply with Europe’s new General Data Protection Regulation (GDPR) that applies since 25 May 2018.