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1. Continuous sensing of IFNα by hepatic endothelial cells shapes a vascular antimetastatic barrier

6. Data from Phosphorylation at Ser-181 of Oncogenic KRAS Is Required for Tumor Growth

9. Supplementary Tables 1 - 3 from Phosphorylation at Ser-181 of Oncogenic KRAS Is Required for Tumor Growth

11. Continuous sensing of IFNα by hepatic endothelial cells shapes a vascular antimetastatic barrier

13. CaM interaction and Ser181 phosphorylation as new K-Ras signaling modulators

14. K-Ras4B phosphorylation at Ser181 is inhibited by calmodulin and modulates K-Ras activity and function

15. A clathrin-dependent pathway leads to KRas signaling on late endosomes en route to lysosomes

16. Phosphorylation at ser-181 of oncogenic KRAS is required for tumor growth

17. Oncogenic K-ras segregates at spatially distinct plasma membrane signaling platforms according to its phosphorylation status

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