Regulation of heterotrimeric G-protein signaling by NDPK/NME proteins and caveolins

• Verfasst von: Abu-Taha, Issam H. [VerfasserIn]
• Verfasst von: Heijman, Jordi [VerfasserIn]
• Verfasst von: Feng, Yuxi [VerfasserIn]
• Verfasst von: Vettel, Christiane [VerfasserIn]
• Verfasst von: Dobrev, Dobromir [VerfasserIn]
• Verfasst von: Wieland, Thomas [VerfasserIn]
• Titel: Regulation of heterotrimeric G-protein signaling by NDPK/NME proteins and caveolins
• Titelzusatz: an update
• Verf.angabe: Issam H. Abu-Taha, Jordi Heijman, Yuxi Feng, Christiane Vettel, Dobromir Dobrev and Thomas Wieland
• Jahr: 2018
• Jahr des Originals: 2017
• Umfang: 8 S.
• Fussnoten: Published 16 October 2017 ; Gesehen am 16.11.2018
• Titel Quelle: Enthalten in: Laboratory investigation
• Ort Quelle: London [u.a.] : Nature Publ. Group, 1996
• Jahr Quelle: 2018
• Band/Heft Quelle: 98(2018), 2, Seite 190-197
• ISSN Quelle: 1530-0307
• DOI: doi:10.1038/labinvest.2017.103
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1581314825

Abstract

Heterotrimeric G proteins are pivotal mediators of cellular signal transduction in eukaryotic cells and abnormal G-protein signaling plays an important role in numerous diseases. During the last two decades it has become evident that the activation status of heterotrimeric G proteins is both highly localized and strongly regulated by a number of factors, including a receptor-independent activation pathway of heterotrimeric G proteins that does not involve the classical GDP/GTP exchange and relies on nucleoside diphosphate kinases (NDPKs). NDPKs are NTP/NDP transphosphorylases encoded by the nme/nm23 genes that are involved in a variety of cellular events such as proliferation, migration, and apoptosis. They therefore contribute, for example, to tumor metastasis, angiogenesis, retinopathy, and heart failure. Interestingly, NDPKs are translocated and/or upregulated in human heart failure. Here we describe recent advances in the current understanding of NDPK functions and how they have an impact on local regulation of G-protein signaling.