Supplementary Materials
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)
Other Supplementary Material for this manuscript includes the following:
- Table S2. Individual-level data corresponding to the different figures (provided as an Excel file).