title: SGK1: The Dark Side of PI3K Signaling.
abstract: Activation of the PI3K pathway is central to a variety of physiological and pathological processes. In these contexts, AKT is classically considered the de facto mediator of PI3K-dependent signaling. However, in recent years, accumulating data point to the existence of additional effectors of PI3K activity, parallel to and independent of AKT, that play critical and unique roles in mediating different developmental, homeostatic, and pathological processes. In this review, I summarize and discuss our current understanding of the function of the serine/threonine kinase SGK1 as a downstream effector of PI3K, and try to separate targets and pathways validated as uniquely SGK1-dependent from those shared with AKT.
authors.affiliation: Albert Einstein College of Medicine, Bronx, NY, United States. Electronic address: antonio.dicristofano@einstein.yu.edu.
authors.forename: Antonio
authors.initials: A
authors.lastname: Di Cristofano
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D047108:Embryonic Development; D004795:Enzyme Stability; D006801:Humans; D017874:Immediate-Early Proteins / Q000378:metabolism*; D009369:Neoplasms / Q000201:enzymology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D015398:Signal Transduction; D000099184:Serum-Glucocorticoid Regulated Kinases
chemical_list: D017874:Immediate-Early Proteins; D019869:Phosphatidylinositol 3-Kinases; D017346:Protein Serine-Threonine Kinases; D000099184:Serum-Glucocorticoid Regulated Kinases
keywords: AGC kinases; AKT; PDK1; PI3K; SGK1