Growth factor-dependent and -independent activation of mTORC2

Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt

Standard

Growth factor-dependent and -independent activation of mTORC2. / Knudsen, Jonas Roland; Fritzen, Andreas Mæchel; James, David E; Jensen, Thomas E; Kleinert, Maximilian; Richter, Erik A.

I: Trends in Endocrinology and Metabolism, Bind 31, Nr. 1, 2020, s. 13-24.

Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt

Harvard

Knudsen, JR, Fritzen, AM, James, DE, Jensen, TE, Kleinert, M & Richter, EA 2020, 'Growth factor-dependent and -independent activation of mTORC2', Trends in Endocrinology and Metabolism, bind 31, nr. 1, s. 13-24. https://doi.org/10.1016/j.tem.2019.09.005

APA

Knudsen, J. R., Fritzen, A. M., James, D. E., Jensen, T. E., Kleinert, M., & Richter, E. A. (2020). Growth factor-dependent and -independent activation of mTORC2. Trends in Endocrinology and Metabolism, 31(1), 13-24. https://doi.org/10.1016/j.tem.2019.09.005

Vancouver

Knudsen JR, Fritzen AM, James DE, Jensen TE, Kleinert M, Richter EA. Growth factor-dependent and -independent activation of mTORC2. Trends in Endocrinology and Metabolism. 2020;31(1):13-24. https://doi.org/10.1016/j.tem.2019.09.005

Author

Knudsen, Jonas Roland ; Fritzen, Andreas Mæchel ; James, David E ; Jensen, Thomas E ; Kleinert, Maximilian ; Richter, Erik A. / Growth factor-dependent and -independent activation of mTORC2. I: Trends in Endocrinology and Metabolism. 2020 ; Bind 31, Nr. 1. s. 13-24.

Bibtex

@article{ed563ad0a64e4a38ab2eda6a5c04eafe,
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 Richter, {Erik A.}",
note = "Copyright {\textcopyright} 2019 Elsevier Ltd. All rights reserved.",
year = "2020",
doi = "10.1016/j.tem.2019.09.005",
language = "English",
volume = "31",
pages = "13--24",
journal = "Trends in Endocrinology and Metabolism",
issn = "1043-2760",
publisher = "Elsevier Ltd. * Trends Journals",
number = "1",

}

RIS

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 A.

N1 - Copyright © 2019 Elsevier Ltd. All rights reserved.

PY - 2020

Y1 - 2020

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

VL - 31

SP - 13

EP - 24

JO - Trends in Endocrinology and Metabolism

JF - Trends in Endocrinology and Metabolism

SN - 1043-2760

IS - 1

ER -

ID: 230036479