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Junyan Shi

Researcher at University of British Columbia

Publications -  23
Citations -  5916

Junyan Shi is an academic researcher from University of British Columbia. The author has contributed to research in topics: Chemistry & Biology. The author has an hindex of 12, co-authored 14 publications receiving 5324 citations. Previous affiliations of Junyan Shi include St. Paul's Hospital.

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Journal Article

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2459 more
- 01 Jan 2016 - 
Journal ArticleDOI

Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

Daniel J. Klionsky, +2522 more
- 01 Jan 2016 - 
TL;DR: Author(s): Klionsky, DJ; Abdelmohsen, K; Abe, A; Abedin, MJ; Abeliovich, H; A Frozena, AA; Adachi, H, Adeli, K, Adhihetty, PJ; Adler, SG; Agam, G; Agarwal, R; Aghi, MK; Agnello, M; Agostinis, P; Aguilar, PV; Aguirre-Ghis
Journal ArticleDOI

Cytoplasmic translocation, aggregation, and cleavage of TDP-43 by enteroviral proteases modulate viral pathogenesis

TL;DR: It is reported that TDP-43 is translocated from the nucleus to the cytoplasm during CVB3 infection through the activity of viral protease 2A, followed by the cleavage mediated by viral proteases 3C, which reveals a mechanism evolved by enteroviruses to support efficient viral infection.
Journal ArticleDOI

Interplay between the cellular autophagy machinery and positive-stranded RNA viruses

TL;DR: The current understanding of how viruses with a positive-stranded RNA genome interact with the host autophagy machinery to control their replication and spread is summarized.
Journal ArticleDOI

Cytoplasmic redistribution and cleavage of AUF1 during coxsackievirus infection enhance the stability of its viral genome

TL;DR: Cytoplasmic redistribution and cleavage of AUF1 during coxsackievirus infection enhance the stability of its viral genome, suggesting an antiviral property forAUF1 against CVB3 infection.