Full text is available at the source.
Getah virus Nsp3 binds G3BP to block formation of bona fide stress granules
Getah virus protein Nsp3 binds G3BP to prevent true stress granule formation
AI simplified
Abstract
GETV infection triggers the formation of Nsp3-G3BP aggregates that differ from typical stress granules.
- Nsp3-G3BP aggregates formed during GETV infection rely on the activation of the PKR/eIF2α signaling pathway.
- The Nsp3 HVD domain inhibits stress granule formation by binding to the G3BP NTF2 domain.
- Knockout of G3BP in NCI-H1299 cells does not affect GETV replication.
- Overexpression of G3BP to create genuine stress granules significantly reduces GETV replication.
- These findings suggest a novel role for GETV Nsp3 in modifying stress granule composition and the cellular stress response.
AI simplified