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. Author manuscript; available in PMC: 2023 Oct 7.
Published in final edited form as: Nature. 2023 Apr 12;617(7960):395–402. doi: 10.1038/s41586-023-05946-4

Fig. 6 ∣. SMAD4 readthrough as endogenous substrate of BAG6.

Fig. 6 ∣

a, The mutation T1657C disrupts SMAD4 stop codon and results in readthrough (RT) translation in the 3’ UTR. b, The SMAD4 readthrough protein is barely detectable in BAG6 wild-type (WT) cells (lane 4) but is stabilized in BAG6 KO cells (lane 5). RT: readthrough with homozygous T1657C mutations. Lane 1: parental WT cells for BAG6 KO. Lane 3: parental WT cells for SMAD4 RT. Bottom: quantification, N=3 biologically independent samples. Data are presented as mean values +/− s.d. c, BAG6 co-IP with SMAD4 readthrough products. Bortezomib: proteasome inhibitor. N=7 biologically independent samples. Data are presented as mean values +/− s.d. Two-sided Student’s t-test was used to calculate P values. No adjustments were made for multiple comparisons. *: P < 0.05; **: P < 0.01.