Skip to main content
. 2014 Aug 4;206(3):347–356. doi: 10.1083/jcb.201404075

Figure 2.

Figure 2.

Effect of gene disruption on chicken gpERAD. (A) RT-PCR to amplify cDNA corresponding to the four α1,2-mannosidase mRNA expressed in DT40 cells of various genotypes. (B) Doubling time of WT and four α1,2-mannosidase KO cells (n = 3). (C) Display of oligosaccharides whose contents in kifunensine (Kif; 10 µg/ml, 6 h)-treated WT DT40 cells and four α1,2-mannosidase KO cells exceeded those in kifunensine-untreated WT cells with an increase over WT (%), as determined from isomer composition of their N-glycans (Fig. S2, A and B), which was completed once. Asterisks denote oligosaccharides whose contents did not exceed those in kifunensine-untreated WT cells. (D) Immunoblotting of cell lysates prepared from kifunensine-untreated or -treated WT DT40 cells and from the four α1,2-mannosidase KO cells using anti-chicken ATF6 (gATF6) antibody. (E) Cycloheximide chase to determine the degradation rate of endogenous gATF6 in kifunensine-untreated or -treated WT DT40 cells and in the four α1,2-mannosidase KO cells (n = 3).