Growth Factor-Dependent and -Independent Activation of mTORC2.

Growth Factor-Dependent and -Independent Activation of mTORC2.
Trends Endocrinol Metab. 2019 Nov 04;:
Authors: Knudsen JR, Fritzen AM, James DE, Jensen TE, Kleinert M, Richter EA
Abstract
The 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.
PMID: 31699566 [PubMed - as supplied by publisher]

Source: Trends in Endocrinology and Metabolism: TEM - November 3, 2019 Category: Endocrinology Authors: Knudsen JR, Fritzen AM, James DE, Jensen TE, Kleinert M, Richter EA Tags: Trends Endocrinol Metab Source Type: research