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The IκB kinase complex is required for plexin-B-mediated activation of RhoA

Plexins are widely expressed transmembrane proteins that mediate the cellular effects of semaphorins. The molecular mechanisms of plexin-mediated signal transduction are still poorly understood. Here we show that signalling via B-family plexins leading to the activation of the small GTPase RhoA requ...

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Hauptverfasser: Zielonka, Matthias (VerfasserIn) , Krishnan, Ramesh K. (VerfasserIn) , Swiercz, Jakub M. (VerfasserIn) , Offermanns, Stefan (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: August 19, 2014
In: PLOS ONE
Year: 2014, Jahrgang: 9, Heft: 8
ISSN:1932-6203
DOI:10.1371/journal.pone.0105661
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1371/journal.pone.0105661
Verlag, lizenzpflichtig, Volltext: https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0105661
Volltext
Verfasserangaben:Matthias Zielonka, Ramesh K. Krishnan, Jakub M. Swiercz, Stefan Offermanns
Beschreibung
Zusammenfassung:Plexins are widely expressed transmembrane proteins that mediate the cellular effects of semaphorins. The molecular mechanisms of plexin-mediated signal transduction are still poorly understood. Here we show that signalling via B-family plexins leading to the activation of the small GTPase RhoA requires activation of the IκB kinase (IKK)-complex. In contrast, plexin-B-dependent regulation of R-Ras activity is not affected by IKK activity. This regulation of plexin signalling depends on the kinase activity of the IKK-complex, but is independent of NF-κB activation. We confirm that the IKK-complex is active in tumour cells and osteoblasts, and we demonstrate that plexin-B-dependent tumour cell invasiveness and regulation of osteoblast differentiation require an active IKK-complex. This study identifies a novel, NF-κB-independent function of the IKK-complex and shows that IKK directs plexin-B signalling to the activation of RhoA.
Beschreibung:Gesehen am 11.09.2020
Beschreibung:Online Resource
ISSN:1932-6203
DOI:10.1371/journal.pone.0105661

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