Skip to main content
. Author manuscript; available in PMC: 2018 Apr 11.
Published in final edited form as: Genet Med. 2017 Aug 17;20(4):411–419. doi: 10.1038/gim.2017.115

Figure 4.

Figure 4

OASIS regulates expression of SEC24D, but not SEC23A. A) SEC23A, encoding a component of the COPII complex, is not significantly upregulated in the presence of WT OASIS under normal conditions. Apparently increased expression in the presence of VT312 OASIS is significant (P=0.03), but given that there is no significant difference in SEC23A expression between WT- and VT312-overexpressing cells, we conclude that SEC23A is not regulated by OASIS. *P <0.05 versus empty vector-transfected control (Tukey Test). RT-qPCR. B) A gene encoding another component of the COPII complex, SEC24D, is significantly upregulated in the presence of WT OASIS (P=0.007 versus empty vector; P=0.009 versus VT312-transfected), but not in the presence of non-functional VT312 OASIS. **P <0.01 versus empty vector-transfected control. ††P <0.01 versus the indicated group (Tukey Test). Y-axes represent relative mRNA expression normalized by the level of GAPDH. Values shown are the mean of three independent experiments (n=3). Error bars, S.D. RT-qPCR. C) Immunoblotting of whole cell lysates from HEK293 overexpressing either WT or VT312 OASIS is consistent with the expression studies, showing that D) the amount of SEC24D protein was augmented upon WT OASIS overexpression, while E) SEC23A protein levels were static.