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Knudsen, J.R.* ; Fritzen, A.M.* ; James, D.E.* ; Jensen, T.E.* ; Kleinert, M. ; Richter, E.A.*

Growth factor-dependent and -independent activation of mTORC2.

Trends Endocrinol. Metab. 31, 13-24 (2020)
DOI
Open Access Green as soon as Postprint is submitted to ZB.
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
Language english
Publication Year 2020
Prepublished in Year 2019
HGF-reported in Year 2019
ISSN (print) / ISBN 1043-2760
e-ISSN 1879-3061
Quellenangaben Volume: 31, Issue: 1, Pages: 13-24 Article Number: , Supplement: ,
Publisher Elsevier
Publishing Place 84 Theobalds Rd, London Wc1x 8rr, England
Reviewing status Peer reviewed
POF-Topic(s) 30201 - Metabolic Health
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-502200-001
Scopus ID 85074714733
Erfassungsdatum 2019-11-25