TY - JOUR A1 - Schröder, Katrin A1 - Weißmann, Norbert A1 - Brandes, Ralf T1 - Organizers and activators : Cytosolic Nox proteins impacting on vascular function T2 - Free radical biology and medicine N2 - NADPH oxidases of the Nox family are important enzymatic sources of reactive oxygen species (ROS) in the cardiovascular system. Of the 7 members of the Nox family, at least three depend for their activation on specific cytosolic proteins. These are p47phox and its homologue NoxO1 and p67phox and its homologue NoxA1. Also the Rho-GTPase Rac is important but as this protein has many additional functions, it will not be covered here. The Nox1 enzyme is preferentially activated by the combination of NoxO1 with NoxA1, whereas Nox2 gains highest activity with p47phox together with p67phox. As p47phox, different to NoxO1 contains an auto inhibitory region it has to be phosphorylated prior to complex formation. In the cardio-vascular system, all cytosolic Nox proteins are expressed but the evidence for their contribution to ROS production is not well established. Most data have been collected for p47phox, whereas NoxA1 has basically not yet been studied. In this article the specific aspects of cytosolic Nox proteins in the cardiovascular system with respect to Nox activation, their expression and their importance will be reviewed. Finally, it will be discussed whether cytosolic Nox proteins are suitable pharmacological targets to tamper with vascular ROS production. KW - Activity control KW - NADPH oxidase KW - Nox KW - NoxA1 KW - NoxO1 KW - Oxygen-derived free radicals KW - Phosphorylation KW - p22phox KW - p47phox KW - p67phox Y1 - 2017 UR - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/45890 UR - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-458906 SN - 1873-4596 SN - 0891-5849 N1 - © 2017 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license (http://creativecommons.org/licenses/BY/4.0/). VL - 109 SP - 22 EP - 32 PB - Elsevier CY - New York, NY [u. a.] ER -