Supplementary Materials

Supplementary Materials for:

Nuclear PTEN enhances the maturation of a microRNA regulon to limit MyD88-dependent susceptibility to sepsis

Flavia Sisti, Soujuan Wang, Stephanie L. Brandt, Nicole Glosson-Byers, Lindsey D. Mayo, Young Min Son, Sarah Sturgeon, Luciano Filgueiras, Sonia Jancar, Hector Wong, Charles S. Dela Cruz, Nathaniel Andrews, Jose Carlos Alves-Filho, Fernando Q. Cunha, C. Henrique Serezani*

*Corresponding author. Email: h.serezan{at}vanderbilt.edu

This PDF file includes:

  • Fig. S1. Antibiotic does not prevent PTEN inhibition–induced animal lethality during sepsis.
  • Fig. S2. PTEN controls MRSA-induced peritonitis.
  • Fig. S3. PTEN protects mice against lung injury during sepsis.
  • Fig. S4. PTEN does not control TRIF-dependent macrophage activation.
  • Fig. S5. PTEN does not dephosphorylate IRAK4 or IKKα in macrophage lysates.
  • Fig. S6. PTEN lipid phosphatase activity decreases MyD88 mRNA and protein abundance in alveolar macrophages.
  • Fig. S7. MyD88-blocking peptide prevents TLR4- and TLR2-mediated, but not TLR3-mediated, nitrite production.
  • Fig. S8. PTEN does not target transcription factors involved in basal Myd88 expression in macrophages.
  • Fig. S9. PTEN controls miRNA abundance in alveolar macrophages.
  • Fig. S10. Differential roles of mTOR and PI3K in miRNA expression.
  • Fig. S11. The miRNAs miR125b and miR203 directly reduce Myd88 mRNA abundance in macrophages.
  • Fig. S12. Efficiency of PTEN-expressing retrovirus in PTEN−/− MEFs.
  • Table S1. Adult sepsis patient demographics.

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