Fig. 5: QKI-7 promoted degradation of CD144, NLGN1, and TSG6 mRNAs.

RNA immunoprecipitation (RIP) was carried out on P014 hiPS-ECs. Significantly more RNAs of CD144, TSG6, and NLGN1 were precipitated by QKI-7 antibody shown by real-time PCR and conventional PCR, indicating the direct binding of QKI-7 to transcripts of these three RNA targets (p values: <0.0001) (a–d). When QKI-7 overexpressing hiPS-ECs or control cells (hiPS-ECs overexpressing an empty vector) were treated with actinomycin D in time point experiments from 0 to 12 h, the QKI-7 overexpression group showed lower mRNA level of CD144, TSG6, and NLGN1 at most of the time points as shown by the mRNA-decay curve, indicating that ectopic QKI-7 promoted mRNA degradation of the three targets (e–g). QKI-7 co-transfection with luciferase reporter plasmid containing wild-type 3′UTR of NLGN1 significantly suppressed the luciferase activity (p value: 0.0329). While this effect was unobservable when QKI-7 was co-transfected with luciferase reporter plasmid containing mutated 3′UTR NLGN1 for the QKI motif (h). Data are from three biologically independent experiments. Error bars represent mean ± SEM (n = 3). P values are shown: *p < 0.05, ****p < 0.0001, ns: not significant (two-tailed t test). Source data are provided as a Source data file.