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P2RY2-driven AKT activation requires p110g, p101, and Ras
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Classroom Contents
Functional Genomic Interrogation of Tumor Evolution
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- 1 Intro
- 2 Research Area 1: Context-dependent regulation of survival signaling in cancer
- 3 Research Area 2: Functional tumor evolution
- 4 Vulnerabilities arising during tumor evolution
- 5 Mapping the beneficial and detrimental effects of selinexor
- 6 AKT activation is a beneficial effect of selinexor
- 7 Selinexor-induced P2RY2 upregulation is necessary and sufficient for AKT activation
- 8 P2RY2-driven AKT activation requires p110g, p101, and Ras
- 9 Antagonistic Pleiotropy: Genes that couple sensitivity and resistance
- 10 Systematic analysis of AP
- 11 A PRC2/NSD/MYC AP axis
- 12 PRC2/MYC dysregulation drives evolved BRD4i resistance
- 13 MYC drives BIM-dependent apoptotic priming and BCL-2 inhibitor sensitivity
