Growth factor-dependent and -independent activation of mTORC2

Jonas Roland Knudsen; Andreas Mæchel Fritzen; David E James; Thomas E Jensen; Maximilian Kleinert; Erik Richter

doi:10.1016/j.tem.2019.09.005

Growth factor-dependent and -independent activation of mTORC2

Jonas Roland Knudsen, Andreas Mæchel Fritzen, David E James, Thomas E Jensen, Maximilian Kleinert, Erik Richter^*

^*Corresponding author for this work

The August Krogh Section for Molecular Physiology

6 Citations (Scopus)

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.

Original language	English
Journal	Trends in Endocrinology and Metabolism
ISSN	1043-2760
DOIs	https://doi.org/10.1016/j.tem.2019.09.005
Publication status	Published - Jan 2020

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10.1016/j.tem.2019.09.005

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title = "Growth factor-dependent and -independent activation of mTORC2",

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.",

author = "Knudsen, {Jonas Roland} and Fritzen, {Andreas M{\ae}chel} and James, {David E} and Jensen, {Thomas E} and Maximilian Kleinert and Erik Richter",

year = "2020",

month = jan,

doi = "10.1016/j.tem.2019.09.005",

language = "English",

journal = "Trends in Endocrinology and Metabolism",

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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

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 -

Growth factor-dependent and -independent activation of mTORC2

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