NoxO1 regulates EGFR signaling by its interaction with Erbin

NADPH oxidase organizer 1 (NoxO1) is a scaffold cytoplasmic subunit of the reactive oxygen species (ROS) forming Nox1 complex and involved in angiogenesis, differentiation, and atherosclerosis. We found that overexpression of NoxO1 without simultaneous overexpression of any other component of the active Nox1 complex inhibited EGF-induced wound closure and signaling, while NoxO1 KO yielded the opposite effect. Accordingly, we hypothesize NoxO1 to exert Nox1 independent functions. Using the BioID technique, we identified ErbB2 interacting protein (Erbin) as novel interaction partner of NoxO1. Colocalization of NoxO1 with EGFR, as well as with Erbin validated this finding. EGF treatment interrupted colocalization of NoxO1 and EGFR. EGF mediated kinase activation was delayed in NoxO1 overexpressing cells, while knockout of NoxO1 had the opposite effect. In conclusion, Erbin was identified as a novel NoxO1 interacting protein. Through the subsequent interaction of NoxO1 and EGFR, NoxO1 interferes with EGF signaling. The results of this study suggest a potential role of NoxO1 as an adaptor protein with functions beyond the well-established enabling of Nox1 mediated ROS formation.

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Publication Details

Journal
Redox Biology
Published
2024-10-17
DOI
https://doi.org/10.1016/j.redox.2024.103396
Citations
5
Primary Topic
Microbial metabolism and enzyme function
Type
article
Field-Weighted Citation Impact
1.17
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article

NoxO1 regulates EGFR signaling by its interaction with Erbin

Katrin Schröder, Tim Schader, Niklas Müller, Manuela Spaeth et al.
5 citations
Redox Biology
Microbial metabolism and enzyme function
1.17
article

NoxO1 regulates EGFR signaling by its interaction with Erbin

Katrin Schröder, Tim Schader, Niklas Müller, Manuela Spaeth, Johannes Graumann, Dana Maureen Hebchen
article en
5 citations

Abstract

NADPH oxidase organizer 1 (NoxO1) is a scaffold cytoplasmic subunit of the reactive oxygen species (ROS) forming Nox1 complex and involved in angiogenesis, differentiation, and atherosclerosis. We found that overexpression of NoxO1 without simultaneous overexpression of any other component of the active Nox1 complex inhibited EGF-induced wound closure and signaling, while NoxO1 KO yielded the opposite effect. Accordingly, we hypothesize NoxO1 to exert Nox1 independent functions. Using the BioID technique, we identified ErbB2 interacting protein (Erbin) as novel interaction partner of NoxO1. Colocalization of NoxO1 with EGFR, as well as with Erbin validated this finding. EGF treatment interrupted colocalization of NoxO1 and EGFR. EGF mediated kinase activation was delayed in NoxO1 overexpressing cells, while knockout of NoxO1 had the opposite effect. In conclusion, Erbin was identified as a novel NoxO1 interacting protein. Through the subsequent interaction of NoxO1 and EGFR, NoxO1 interferes with EGF signaling. The results of this study suggest a potential role of NoxO1 as an adaptor protein with functions beyond the well-established enabling of Nox1 mediated ROS formation.

Redox BiologyVol. 77
Goethe University Frankfurt (DE), Max Planck Institute for Heart and Lung Research (DE)
Zero hunger
Openalex Percentile: Top 21%
Microbial metabolism and enzyme function
1.17
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NoxO1 regulates EGFR signaling by its interaction with Erbin — Katrin Schröder, Tim Schader, et al. · Redox Biology (2024) | TGRS Research Map | TGRS