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Fig. 4 | Journal of Translational Medicine

Fig. 4

From: Transcriptomics-proteomics Integration reveals alternative polyadenylation driving inflammation-related protein translation in patients with diabetic nephropathy

Fig. 4

The potential regulation mechanisms of PAS selection and translation enhancement in DN. a The protein scatterplots of the representative polyadenylation factors (NUDT21, CPSF6, SNRNP70, PABPC1 and CstF64) between DN patients and control subjects. b The number of genes gaining RBP-binding sites due to the lengthening of 3′UTR. 77% 3′UTR lengthened genes have gained at least one predicted RBP binding site. c The schematic of 3′UTR lengthening increasing gene translation in DN. Genes such as CYB5R1 and PDLIM1 preferred the use of proximal PAS under normal conditions. In DN, upregulated polyadenylation factors (NUDT21, CPSF6, SNRNP70, and PABPC1) resulted in higher usage of distal PASs and thus increased the abundance of the isoform with longer 3′UTR, which produced more protein through gaining more RBP binding sites

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