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Supplementary Materials

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  • fig. S1. Generation of RIG-I KO and its mutant-rescued cell lines.
  • fig. S2. RIG-I8KR failed to induce ISG expression as well as the antiviral capability.
  • fig. S3. Ubiquitination and functional assays support the stratified mechanism of RIG-I–N multisite ubiquitination.
  • fig. S4. Antiviral capability of various RIG-I mutants.
  • fig. S5. K172R mutation of RIG-I does not influence conjugated ubiquitination of RIG-I but strongly impairs RIG-I unanchored ubiquitination.
  • fig. S6. The expression patterns of ISGs induced by RIG-IWT, RIG-IK164R, and RIG-IK172R do not show obvious difference.
  • fig. S7. Illustration of RIG-I oligomerization detection system.
  • fig. S8. Steady state of poly(I:C)-induced type I IFN activation in RIG-IWT 293T cells.
  • fig. S9. Mathematical analysis data fit experimental results well.
  • fig. S10. Dynamics of the protein levels of E3 ligases show subtle difference on the ultrasensitivity of RIG-I activation.
  • fig. S11. Transcriptome analysis of RIG-IWT, RIG-IK164R, RIG-IK172R, and RIG-I6KR reconstructed cells.
  • fig. S12. Dendrograms for randomness in gene expression under RIG-IWT and RIG-I6KR conditions.
  • fig. S13. ISG inductions in each cluster.
  • fig. S14. Function of E3 ligases in RIG-I–induced type I IFN activation and the knockdown efficiency of indicated E3 ligase’s siRNAs.
  • fig. S15. Steady state of RIG-I–induced type I IFN activation in WT 293T cells.
  • fig. S16. Activation slope of transcription factors and transcription factor kinases during SeV infection.
  • table S1. Parameter values in the model.
  • table S2. The number of equations and different ubiquitinated RIG-I that can form tetramers under different conditions.
  • Supplementary Methods
  • References (40–48)

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