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Open Access Green as soon as Postprint is submitted to ZB.
Growth factor-dependent and -independent activation of mTORC2.
Trends Endocrinol. Metab. 31, 13-24 (2020)
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.
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Publication type
Article: Journal article
Document type
Review
Keywords
Activation Mechanisms ; Exercise. ; Mtorc2 ; Subcellular Localization; Complex 2 Mtorc2; Mammalian Target; Glucose-uptake; Phosphatidic-acid; Membrane Localization; Protein Complexes; Phosphoinositide 3-kinase; Motif Phosphorylation; Endoplasmic-reticulum; Akt Phosphorylation
ISSN (print) / ISBN
1043-2760
e-ISSN
1879-3061
Quellenangaben
Volume: 31,
Issue: 1,
Pages: 13-24
Publisher
Elsevier
Publishing Place
84 Theobalds Rd, London Wc1x 8rr, England
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes and Obesity (IDO)