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Trautenberg, L.C.* ; Prince, E.* ; Maas, C.* ; Beier, N.* ; Honold, F.* ; Grzybek, M. ; Brankatschk, M.*

Selective phosphorylation of Akt/Protein-kinase B isoforms in response to dietary cues.

Front. Cell Dev. Biol. 7:206 (2019)
Publ. Version/Full Text Research data DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
A calorie-rich diet is one reason for the continuous spread of metabolic syndromes in western societies. Smart food design is one powerful tool to prevent metabolic stress, and the search for suitable bioactive additives is a continuous task. The nutrient-sensing insulin pathway is an evolutionary conserved mechanism that plays an important role in metabolism, growth and development. Recently, lipid cues capable to stimulate insulin signaling were identified. However, the mechanistic base of their activity remains obscure to date. We show that specific Akt/Protein-kinase B isoforms are responsive to different calorie-rich diets, and potentiate the activity of the cellular insulin cascade. Our data add a new dimension to existing models and position Drosophila as a powerful tool to study the relation between dietary lipid cues and the insulin-induced cellular signal pathway.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Drosophila ; Saccharomyces Cerevisiae ; Cystobasidium Oligophagum ; Akt ; Pkb ; Akt Phosphorylation ; Insulin Signaling ; Yeast Lipids; Drosophila Insulin-receptor; Signaling Pathway; Growth; Acid; Cell; Akt; Yeast; Homeostasis; Activation; Mechanism
Language english
Publication Year 2019
HGF-reported in Year 2019
ISSN (print) / ISBN 2296-634X
e-ISSN 2296-634X
Journal Frontiers in cell and developmental biology
Quellenangaben Volume: 7, Issue: , Pages: , Article Number: 206 Supplement: ,
Publisher Frontiers
Publishing Place Lausanne
Reviewing status Peer reviewed
Institute(s) Institute of Pancreatic Islet Research (IPI)
POF-Topic(s) 90000 - German Center for Diabetes Research
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-502600-002
DOI 10.3389/fcell.2019.00206
WOS ID WOS:000497384200001
Scopus ID 85074177956
PubMed ID 31649929
Erfassungsdatum 2019-11-04
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