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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 Verlagsversion bestellen
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter 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 Band: 31, Heft: 1, Seiten: 13-24 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort 84 Theobalds Rd, London Wc1x 8rr, England
Begutachtungsstatus Peer reviewed