Fig. 8: Molecular basis for 2A-induced reprogramming of gene expression. | Nature Communications

Fig. 8: Molecular basis for 2A-induced reprogramming of gene expression.

From: Structural and molecular basis for Cardiovirus 2A protein as a viral gene expression switch

Fig. 8

The PRF stimulatory RNA element is predicted to form either stem-loop or pseudoknot conformations. As 2A accumulates during EMCV infection, it selectively binds to and stabilises a pseudoknot-like conformation of the PRF stimulatory element, thereby enabling PRF, producing trans-frame product 2B* and downregulating the expression of enzymatic viral proteins later in infection. 2A also binds directly to the small ribosomal subunit at the translational GTPase factor binding site, progressively inhibiting both initiation and elongation as it accumulates. This may contribute to the shutdown of host cell translation during lytic infection.

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