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. 2024 Mar 19;121(13):e2309925121. doi: 10.1073/pnas.2309925121

Fig. 3.

Fig. 3.

hA3G cooperates with HBZ to activate the TGF-β/SMAD pathway. (A) Expression of hA3G in healthy donors (n = 9) and patients with aggressive ATL (acute, and lymphoma type ATL) (n = 20) by RT-qPCR (triplicate experiments; one-way ANOVA with Tukey correction; ***P < 0.001). (B) Gene signatures that are significantly enriched in hA3G-knockdown ATL cells (ATL-55T+), based on GSEA analysis with RNA-seq. (C) Luciferase activity of 3TP-Lux under the control of a TGF-β responsive element in cells expressing hA3G or sA3G (normalized mean ± SD of triplicate experiments; two-tailed unpaired Student’s t test; **P < 0.01; ***P < 0.001). (D) Luciferase activity of 3TP-Lux under the control of a TGF-β responsive element in cells coexpressing HBZ with hA3G (Left), APH-2 with hA3G (Middle), or SBZ with sA3G (Right) (normalized mean ± SD of triplicate experiments; two-tailed unpaired Student’s t test; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001). (E) Luciferase activity of 3TP-Lux under the control of a TGF-β responsive element in cells expressing deletion mutants of the N-terminal region of hA3G (normalized mean ± SD of triplicate experiments; two-tailed unpaired Student’s t test; ***P < 0.001). IB, immunoblot. (F) Luciferase activity of 3TP-Lux under the control of a TGF-β responsive element in cells expressing alanine scanning mutants of the 12 to 18th amino acids of hA3G (normalized mean ± SD of triplicate experiments; two-tailed unpaired Student’s t test; ****P < 0.0001). IB, immunoblot.