TY - JOUR
T1 - Growth factor-dependent and -independent activation of mTORC2
AU - Knudsen, Jonas Roland
AU - Fritzen, Andreas Mæchel
AU - James, David E
AU - Jensen, Thomas E
AU - Kleinert, Maximilian
AU - Richter, Erik
N1 - Copyright © 2019 Elsevier Ltd. All rights reserved.
PY - 2020/1
Y1 - 2020/1
N2 - 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.
AB - 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.
U2 - 10.1016/j.tem.2019.09.005
DO - 10.1016/j.tem.2019.09.005
M3 - Review
C2 - 31699566
SN - 1043-2760
JO - Trends in Endocrinology and Metabolism
JF - Trends in Endocrinology and Metabolism
ER -