Supplementary Material for:

ALK is a therapeutic target for lethal sepsis

Ling Zeng, Rui Kang, Shan Zhu, Xiao Wang, Lizhi Cao, Haichao Wang, Timothy R. Billiar, Jianxin Jiang,* Daolin Tang*

*Corresponding author. Email: tangd2{at}upmc.edu (D.T.); jiangjx{at}cta.cq.cn (J.J.)

Published 18 October 2017, Sci. Transl. Med. 9, eaan5689 (2017)
10.1126/scitranslmed.aan5689

This PDF file includes:

• Materials and Methods
  
• Fig. S1. ALK inhibitors block STING activation.
  
• Fig. S2. Pharmacologic inhibition of ALK blocks STING ligand–induced IFNβ release and expression.
  
• Fig. S3. Pharmacologic inhibition of ALK blocks STING activation.
  
• Fig. S4. Genetic inhibition of ALK limits STING activation.
  
• Fig. S5. ALK does not bind known STING regulators.
  
• Fig. S6. Inhibition of ALK limits RTK phosphorylation in STING activation.
  
• Fig. S7. ALK binds EGFR during STING activation.
  
• Fig. S8. The ALK-EGFR-AKT pathway mediates STING activation.
  
• Fig. S9. Knockdown of EGFR inhibits STING activation.
  
• Fig. S10. The ALK-EGFR-AKT pathway mediates STING ligand–induced IFNβ release and expression.
  
• Fig. S11. ALK mediates LPS-induced macrophage activation.
  
• Fig. S12. Histological analysis of tissue injury in CLP-treated mice.
  
• Fig. S13. Heatmap of circulating immune chemical profile in indicated mice.
  
• Fig. S14. Histological analysis of tissue injury in LPS-treated mice.
  
• Fig. S15. Heatmap of circulating immune chemical profile in indicated mice.
  
• Fig. S16. Effects of targeting the ALK-STING pathway on CLP-induced septic death.
  
• Fig. S17. Schematic depicting the pathologic role of ALK-dependent STING pathways in lethal sepsis.
  
• Table S1. Reagent sources.
  
• Reference (70)

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Other Supplementary Material for this manuscript includes the following:

• Table S2. Individual-level data corresponding to the different figures (provided as an Excel file).