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Alexander Martin Heberle
Researcher at University Medical Center Groningen
Publications - 18
Citations - 719
Alexander Martin Heberle is an academic researcher from University Medical Center Groningen. The author has contributed to research in topics: mTORC1 & PI3K/AKT/mTOR pathway. The author has an hindex of 7, co-authored 13 publications receiving 561 citations. Previous affiliations of Alexander Martin Heberle include University of Innsbruck.
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Journal ArticleDOI
A systems study reveals concurrent activation of AMPK and mTOR by amino acids
Piero Dalle Pezze,Stefanie Ruf,Stefanie Ruf,Annika G Sonntag,Miriam Langelaar-Makkinje,Philip Hall,Alexander Martin Heberle,Patricia Razquin Navas,Patricia Razquin Navas,Karen van Eunen,Regine C Tölle,Jennifer J. Schwarz,Heike Wiese,Bettina Warscheid,Jana Deitersen,Björn Stork,Erik Fäßler,Sascha Schäuble,Udo Hahn,Peter Horvatovich,Daryl P. Shanley,Kathrin Thedieck,Kathrin Thedieck +22 more
TL;DR: It is found that aa acutely activate AMPK concurrently with mTOR, and it is shown that AMPK under aa sufficiency acts to sustain autophagy, which may be required to maintain protein homoeostasis and deliver metabolite intermediates for biosynthetic processes.
Journal ArticleDOI
Molecular mechanisms of mTOR regulation by stress
Alexander Martin Heberle,Mirja Tamara Prentzell,Karen van Eunen,Barbara M. Bakker,Sushma Nagaraja Grellscheid,Kathrin Thedieck +5 more
TL;DR: An overview of the mechanisms contributing to mTOR regulation by stress is provided and a model wherein stress granules function as guardians of mTORC1 signaling, allowing cancer cells to escape stress-induced cell death is suggested.
Journal ArticleDOI
PLK1 (polo like kinase 1) inhibits MTOR complex 1 and promotes autophagy
Stefanie Ruf,Alexander Martin Heberle,Miriam Langelaar-Makkinje,Sara Gelino,Deepti S. Wilkinson,Carolin Gerbeth,Jennifer J. Schwarz,Birgit Holzwarth,Bettina Warscheid,Chris Meisinger,Marcel A. T. M. van Vugt,Ralf Baumeister,Malene Hansen,Kathrin Thedieck +13 more
TL;DR: It is proposed that cautious monitoring of MTORC1 and autophagy readouts in clinical trials with PLK1 inhibitors is needed to develop strategies for optimized (combinatorial) cancer therapies targeting MT ORC1, PLK 1, and autophileagy.
Journal ArticleDOI
G3BPs tether the TSC complex to lysosomes and suppress mTORC1 signaling
Mirja Tamara Prentzell,Ulrike Rehbein,Ulrike Rehbein,Ulrike Rehbein,Marti Cadena Sandoval,Marti Cadena Sandoval,Ann-Sofie De Meulemeester,Ralf Baumeister,Laura Brohée,Bianca Berdel,Mathias Bockwoldt,Bernadette Carroll,Suvagata Roy Chowdhury,Andreas von Deimling,Andreas von Deimling,Constantinos Demetriades,Constantinos Demetriades,Gianluca Figlia,Gianluca Figlia,Mariana E. G. de Araujo,Alexander Martin Heberle,Alexander Martin Heberle,Ines Heiland,Birgit Holzwarth,Lukas A. Huber,Jacek Jaworski,Magdalena Kedra,Katharina Kern,Andrii Kopach,Viktor I. Korolchuk,Ineke van 't Land-Kuper,Ineke van 't Land-Kuper,Matylda Macias,Mark Nellist,Wilhelm Palm,Stefan Pusch,Stefan Pusch,Jose Miguel Ramos Pittol,Michèle Reil,Anja Reintjes,Friederike Reuter,Julian R. Sampson,Chloë Scheldeman,Aleksandra Siekierska,Eduard Stefan,Aurelio A. Teleman,Aurelio A. Teleman,Laura E. Thomas,Omar Torres-Quesada,Saskia Trump,Hannah West,Peter de Witte,Sandra Woltering,Teodor E. Yordanov,Teodor E. Yordanov,Justyna Zmorzynska,Christiane A. Opitz,Christiane A. Opitz,Kathrin Thedieck,Kathrin Thedieck,Kathrin Thedieck +60 more
TL;DR: In this article, GTPase-activating protein-binding proteins 1 and 2 (G3BP1 and G3BP2, respectively) are reported to reside at the cytoplasmic surface of lysosomes.
Journal ArticleDOI
The PI3K and MAPK/p38 pathways control stress granule assembly in a hierarchical manner
Alexander Martin Heberle,Patricia Razquin Navas,Patricia Razquin Navas,Miriam Langelaar-Makkinje,Katharina Kasack,Katharina Kasack,Ahmed Sadik,Ahmed Sadik,Erik Faessler,Udo Hahn,Philip Marx-Stoelting,Christiane A. Opitz,Christine Sers,Christine Sers,Ines Heiland,Sascha Schäuble,Sascha Schäuble,Kathrin Thedieck,Kathrin Thedieck,Kathrin Thedieck +19 more
TL;DR: A new pro-survival function is assigned to the key oncogenic kinases PI3K and p38, as they hierarchically promote stress granule formation as well as the metabolic master regulator mammalian target of rapamycin complex 1.