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. 2018 Jul 17;92(15):e00431-18. doi: 10.1128/JVI.00431-18

FIG 1.

FIG 1

TGEV infection induces ER stress in ST and IPEC-J2 cells. ST cells and IPEC-J2 cells were infected with TGEV H87 at an MOI of 1; samples were collected at 0, 6, 12, 24, 36, and 48 hpi. (A) One-step growth curve of TGEV in ST cells and IPEC-J2 cells. (B) A time-dependent increase of GRP78 expression was revealed by qPCR in ST cells and IPEC-J2 cells. Total RNA was isolated, and the transcriptional levels of GRP78 were measured by qPCR at different time points (0 to 48 h) after infection. (C) Elevated protein expression of GRP78 was confirmed by Western blotting in ST cells and IPEC-J2 cells. Tu (2 μg/ml) was used as a positive control for UPR activation; β-actin was used as a loading control. (D) Relative GRP78 levels. (E) TGEV-induced UPR was dependent on active viral replication. ST cells were infected with UV-inactivated TGEV or treated with Tu (2 μg/ml). The GRP78 expression in ST cells at different time points was determined by Western blotting using anti-GRP78 antibody. (F) Relative GRP78 levels. Means and SD of the results from three independent experiments are shown.