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. Author manuscript; available in PMC: 2021 Sep 25.
Published in final edited form as: Nat Immunol. 2021 Mar 25;22(4):423–433. doi: 10.1038/s41590-021-00898-1

Extended Data Fig. 6. NLRX1 promotion of HIV-1 replication in CD4 T cells is independent of IFN-I, autophagy, or ER stress.

Extended Data Fig. 6

a. RLU in Jurkat sh-Ctr or sh-NLRX1 cells infected with VSV-G-NL4–3-Luc (MOI=1) or left uninfected in the presence or absence of JAK1/2 inhibitor Ruxolitinib at 24 hpi. n = 3 cell cultures per experiment.

b. Ruxolitinib suppressed VSV-G-NL4–3-Luc infection-induced phosphorylation of STAT1 at 24 hpi. β-actin was used as the loading control.

c. Similar to a except for using autophagy inhibitor 3-Methyladenine‎ (3-MA) to treat cells. Numbers on top of the bar are the fold differences. n = 3 cell cultures per experiment.

d. Similar to a except for using ER stress inhibitor sodium tauroursodeoxycholate (TUDCA) to treat cells. Luciferase activities were determined at 48 hpi. n = 3 cell cultures per experiment.

Representative data of three independent experiments are presented as the mean ± s.e.m. Two-way ANOVA followed by Sidak’s multiple comparisons test.