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Article Addendum
The Heterotrimeric G Protein Gi3 Regulates Hepatic Autophagy Downstream of the Insulin Receptor
Antje Gohla, Karinna Klement and Bernd Nürnberg
volume 3 | issue 4
July/August 2007Pages: 393 - 395
This is an open-access article
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Compelling evidence suggests that the heterotrimeric G protein Gi3 specifically transmits the antiautophagic effects of insulin and amino acids in the liver. This points to a previously unrecognized cross talk between the insulin receptor tyrosine kinase and Gi3. Interestingly, Gi3 is localized not only to plasma membranes but also to membranes of the autophagosomal compartment. Furthermore, as part of insulin’s or phenylalanine’s actions to inhibit autophagy, Gi3 is redistributed away from autophagosomes. Therefore, endomembrane-associated rather than plasma membrane-localized Gi3 may serve as the target of insulin’s endocrine and metabolic actions. We therefore propose that the function and regulation of organelle-associated heterotrimeric G proteins may be different from their roles at the plasma membrane where they act as signal transducers of seven-transmembrane receptors. Here, we discuss recent findings and propose a function for Gi3 in mTOR-dependent signaling pathways. We hypothesize that Gi family members may have tissue-specific roles in the regulation of autophagy under different physiological and pathological conditions.
Addendum to:
An Obligatory Requirement for the Heterotrimeric G Protein Gi3 in the Antiautophagic Action of Insulin in the Liver
A. Gohla, K. Klement, R.P. Piekorz, K. Pexa, S. vom Dahl, K. Spicher, V. Dreval, D. Häussinger, L. Birnbaumer and B. Nürnberg
Proc Natl Acad Sci USA 2007; 104:3003-8
Authors
Antje Gohla
Heinrich-Heine-Universitaet
Karinna Klement
Heinrich-Heine-University
Bernd Nürnberg
Clinic for Dermatology, Venerology and Allergology, The Saarland University Hospital
This is an open-access article
Download PDFIf the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.