Supplementary Materials

The PDF file includes:

  • Fig. S1. Schematic of pairwise comparisons of microarray data.
  • Fig. S2. A persistent small increase in NOD1 leads to its oligomerization and inflammatory gene expression.
  • Fig. S3. A persistent small increase in NOD1 expression leads to saturating expression of proto-oncogenes.
  • Fig. S4. Tolerization of ligand-responsive genes after repeated NOD1 activation with ligand.
  • Fig. S5. CRISPR-Cas9–mediated ablation of FLAG-NOD1 and RIPK2 in THP-1 NOD1 cells.
  • Fig. S6. miR-15b, miR-16, and miR-106a control NOD1 expression specifically in human cells.
  • Fig. S7. Validation of CRISPR-Cas9–targeted editing of miR-15b/16.
  • Fig. S8. Proposed consequences of a small increase in NOD1 expression.
  • Table S1. List of primers and probes used for evaluating expression of endogenous and 3X-FLAG–tagged NOD1 and NLRP4 by qPCR.
  • Table S2. Details of genome-wide microarray expression datasets analyzed in Fig. 3.
  • Legends for data files S1 to S3
  • Reference (46)

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Other Supplementary Material for this manuscript includes the following:

  • Data file S1 (Microsoft Excel format). KEGG pathways up-regulated by NOD1 and NLRP4 under conditions of low-level (− DOX) or DOX-induced expression.
  • Data file S2 (Microsoft Excel format). Proinflammatory genes associated with a ligand-induced NOD1 response are up-regulated in cells with a small increase in NOD1 but not in cells with a small increase in NLRP4 expression.
  • Data file S3 (Microsoft Excel format). List of miRNAs on the Affymetrix GeneChip Human 1.0 ST microarray showing correlation of miRNAs with NOD1 and their predicted binding to the NOD1 3′UTR.