Fig. 1
From: A review of mechanisms of disease across PIK3CA-related disorders with vascular manifestations
The PI3K signaling pathway and inhibitors under investigation. Because PIK3CA mutations underlie the pathogenesis of PIK3CA-related disorders, there are multiple strategies for targeting the PI3K pathway under investigation [6, 8]. AKT: protein kinase B; AMP: adenosine monophosphate; AMPK: AMP-activated protein kinase; ATP: adenosine triphosphate; BAD: Bcl-2-associated death promoter; CDC42: Cell division control protein 42 homolog; ERK: extracellular signal regulated kinase; FKHR: forkhead; GDP: guanosine diphosphate; GPCR, G protein-coupled receptor; Grb2: growth factor receptor-bound protein 2; GSK3: glycogen synthase kinase 3; GTP: guanosine-5'-triphosphate; IRS: insulin receptor substrate; LKB1: liver kinase B1; MAPK: mitogen-activated protein kinase; MDM2: mouse double minute 2; mTOR: mammalian target of rapamycin; NF-κB: nuclear factor kappa B; P: phosphate; PI3K: phosphatidylinositol-3-kinase; PIK3CA: phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; PIP2: phosphatidylinositol-4,5-bisphosphate; PIP3: phosphatidylinositol-3,4,5-triphosphate; PKA: protein kinases A; PKC: protein kinase C; PROS: PIK3CA-related overgrowth spectrum; PTEN: phosphatase and tensin homolog; RAC1: Ras-related C3 botulinum toxin substrate 1; Ras: rat sarcoma; RTK, receptor tyrosine kinase; SGK: serum- and glucocorticoid-inducible kinase; Src: rous sarcoma; TIE2, angiopoietin-1 receptor. Adapted with permission from Hennessy 2005 [7]