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. 2019 Jun 5;12(6):dmm039602. doi: 10.1242/dmm.039602

Fig. 6.

Fig. 6.

NGI-1 treatment of transfected HEK cells results in underglycosylation of both furin and PCSK5, leading to more penetrant receptor-processing defects. (A) Representative western blots of HEK WT and 10 µM NGI-1-treated cells transfected with Flag-tagged murine constructs for PCSK5a and furin (n=3). (B) Quantification of the level of pro-receptor relative to the total amount of receptor (pro-receptor+mature receptor) of three biological replicates. Error bars represent s.e.m. (C) Representative western blot from three separate experiments of HEK WT and NGI-1-treated cells transfected with Flag-tagged murine constructs for PCSK5a and furin in untreated and PNGase-F-treated cell lysates. (D) Quantitative PCR analysis of the transcript abundance of PCSK5a and furin in HEK WT and NGI-1-treated cells. **P<0.01, ***P<0.001.