Fig. 4: Loss of SMYD5-RPL40 K22me3 axis leads to elongation perturbation and hypersensitivity to translation inhibitors targeting A-site. | Cell Research

Fig. 4: Loss of SMYD5-RPL40 K22me3 axis leads to elongation perturbation and hypersensitivity to translation inhibitors targeting A-site.

From: SMYD5 is a ribosomal methyltransferase that catalyzes RPL40 lysine methylation to enhance translation output and promote hepatocellular carcinoma

Fig. 4

a Polysome profiles from lysates with RNase A treatment of NC and SMYD5 KO1 Huh7 cell lines. Black arrows denote the disomes. b, c WB analyses for phosphorylation of p38 in the NC and SMYD5 KO1 Huh7 cell lines treated with ANS (0.001–1 mg/L, 15 min) or Harringtonine (HT) (0.1–10 μM, 15 min). d, e WB analyses for phosphorylation of p38 in the NC and SMYD5 KO1 Huh7 cell lines treated with ANS (0.01–1 mg/L, 15 min) or HT(10 μM, 15 min). Before ANS or HT treatment, the NC and SMYD5 KO1 Huh7 cell lines were treated with DMSO or ZAK inhibitor M443 (5 μM, 1 h) as indicated. Note: α-Tubulin was used as a control for panels in all above and below WB analyses.

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