Supplementary Materials

The PDF file includes:

  • Methods
  • Fig. S1. Chemical structures of compounds used in this study.
  • Fig. S2. Screening the PKIS collection identifies the CMGC kinase family.
  • Fig. S3. CDK family inhibitor screen.
  • Fig. S4. Selectivity of the probes designed to recognize the SNP within DMPK.
  • Fig. S5. ddPCR used in aberrant splicing analysis.
  • Fig. S6. HSALR muscle pathology and EMG analysis following dinaciclib treatment.
  • Fig. S7. Comparison of protein binding profiles for immobilized inhibitors SNS-032 and AT7519.
  • Fig. S8. CDK family member proteins identified by whole proteome analysis of DM1 fibroblasts.
  • Fig. S9. Dose-response competition-binding curves for different compound/target combinations.
  • Fig. S10. CDK12 protein knockdown by siRNA and shRNA.
  • Fig. S11. THZ531 foci removal in DM1 fibroblast cells.
  • Fig. S12. Dynamics of the accumulation and degradation of CUG960 and eGFP transcripts.
  • Table S1. pIC50 values in the nuclear foci assay of six PKIS hit compounds in two DM1 cell lines.
  • Table S2. IC50 values (nM) of previously reported CDK inhibitors.
  • Table S3. Kinobeads profiling of a set of 11 compounds that represent a range of activities in the nuclear foci assay.
  • Table S4. pIC50 values generated by affinity capturing with the SNS-032 affinity matrix in K562 cell extract for the different CDK inhibitors added to the cell extracts.
  • Table S5. Dual-labeled probes used in ddPCR assays.
  • Table S6. Primers used in ddPCR assays.
  • Legends for data files S1 to S3
  • References (5572)

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). Proteomic raw data.
  • Data file S2 (Microsoft Excel format). Whole proteome and CZC188 beads DM versus non-DM fibroblasts.
  • Data file S3. (Excel document): Raw data and statistical details for Figs. 1 to 5.