Junyan Shi

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: In this paper, the patho-stratagems of coxsackievirus B3 are explored from molecular, and systems-level approaches, focusing particularly on mechanisms by which CVB3 can harness different host cell processes including kinases, host cell-killing and cell-eating machineries, matrix metalloproteinases and miRNAs to promote disease.

TL;DR: The results suggest a novel model by which cleavage of SQSTM1 as a result of CVB3 infection impairs the function of SQ STM1 in selective autophagy and host defense signaling.

TL;DR: This study reveals a mechanism that supports an emerging model whereby CVB3 hijacks the autophagic machinery to facilitate its own propagation, and demonstrates that loss of SNAP29/PLEKHM1 inhibits Autophagic flux, resulting in increased viral replication.

TL;DR: The studies demonstrated that SGs were formed early during CVB3 infection; however, G3BP1-positiveSGs were actively disassembled at 5 hrs post-infection, while poly(A)-positive RNA granules persisted, and evidence that the C-terminal cleavage product of G3 BP1 inhibited SG formation and promotedCVB3 replication was provided.