Growth Factor-Dependent and -Independent Activation of mTORC2

Publication date: Available online 4 November 2019Source: Trends in Endocrinology & MetabolismAuthor(s): Jonas R. Knudsen, Andreas M. Fritzen, David E. James, Thomas E. Jensen, Maximilian Kleinert, Erik A. RichterThe target of rapamycin complex 2 (TORC2) was discovered in 2002 in budding yeast. Its mammalian counterpart, mTORC2, was first described in 2004. Soon thereafter it was demonstrated that mTORC2 directly phosphorylates Akt on Ser473, ending a long search for the elusive ‘second’ insulin-responsive Akt kinase. In this review we discuss key evidence pertaining to the subcellular localization of mTORC2, highlighting a spatial heterogeneity that relates to mTORC2 activation. We summarize current models for how growth factors (GFs), such as insulin, trigger mTORC2 activation, and we provide a comprehensive discussion focusing on a new exciting frontier, the molecular mechanisms underpinning GF-independent activation of mTORC2.

Source: Trends in Endocrinology and Metabolism - November 5, 2019 Category: Endocrinology Source Type: research