Short RNA Duplexes Elicit RIG-I–Mediated Apoptosis in a Cell Type– and Length-Dependent Manner

Osamu Ishibashi, Md. Moksed Ali, Shan-Shun Luo, Takashi Ohba, Hidetaka Katabuchi, Toshiyuki Takeshita, Toshihiro Takizawa*

*To whom correspondence should be addressed. E-mail: t-takizawa{at}nms.ac.jp

This PDF file includes:

• Fig. S1. Pre-351 reduced the viability of KGN cells regardless of the transfection method used.
• Fig. S2. Sequences of miRs-125b, -351, and -125a-5p.
• Fig. S3. Dose-dependent effect of poly(I:C) on KGN cell viability.
• Fig. S4. Effects of pre-miRs on HL-60 cell viability.
• Fig. S5. Pre-351–induced apoptosis of GC1 cells.
• Fig. S6. Subcellular translocation of cytochrome c and NF-κB in KGN cells transfected with Pre-351.
• Fig. S7. Pre-351 reduced the viability of KGN cells in an IFN-independent manner.
• Fig. S8. MDA5 is not involved in Pre-351–induced apoptosis of KGN cells.
• Fig. S9. siRNA-mediated knockdown of RIG-I in KGN cells.
• Fig. S10. The transcriptional induction of a representative ISG (MX1) by Pre-351 was mostly unaffected by knockdown of RIG-I.
• Fig. S11. Pretreatment of HeLa cells with IFN-β potentiated the ability of Pre-351 to enhance caspase-3 and caspase-7 activities.
• Fig. S12. Knockdown of RIG-I in HuCCT1 cells by siRNA.
• Fig. S13. Pre-351 induced the phosphorylation of p38 in KGN cells.
• Fig. S14. PKRI- and RIG-I–dependent Pre-351–induced phosphorylation of p38.
• Fig. S15. Basal abundance of RIG-I mRNA in KGN and HeLa cells.
• Fig. S16. Schematic model of short dsRNA–induced apoptotic signaling mediated by PKR, RIG-I, and p38 MAPK.
• Table S1. Genes whose expression was increased (>50-fold) in KGN cells after transfection with Pre-351 as compared to their expression in cells transfected with Pre-Cont.
• Table S2. List of siRNAs used in this study.
• Table S3. Primers used for real-time PCR analysis.

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© 2011 American Association for the Advancement of Science