Synergistica activation of NF-κB by functional cooperation between Vav and PKCθ in T lymphocytes

<p>Here we identified PKCθ as an activator of transcription factor NF-κB in T cells. PKCθ-induced NF-κB activation was synergistically augmented by Vav. Several experimental approaches revealed that PKCθ is located downstream from Vav in the control of the pathway leading to synergistic NF-κB...

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Hauptverfasser: Dienz, Oliver (VerfasserIn) , Dröge, Wulf (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: June 21, 2000
In: The journal of biological chemistry
Year: 2000, Jahrgang: 275, Heft: 32, Pages: 24547-24551
ISSN:1083-351X
DOI:10.1074/jbc.C000177200
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1074/jbc.C000177200
Verlag, lizenzpflichtig, Volltext: https://www.jbc.org/article/S0021-9258(19)62205-2/abstract
Volltext
Verfasserangaben:Oliver Dienz, Steffen P. Hehner, Wulf Dröge, and M. Lienhard Schmitz
Beschreibung
Zusammenfassung:<p>Here we identified PKCθ as an activator of transcription factor NF-κB in T cells. PKCθ-induced NF-κB activation was synergistically augmented by Vav. Several experimental approaches revealed that PKCθ is located downstream from Vav in the control of the pathway leading to synergistic NF-κB activation. In addition to the synergistic activation cascade, Vav also triggered NF-κB activity on a separate route. CD3/CD28-induced activation of NF-κB was inhibited by dominant negative forms of Vav or PKCθ, revealing their essential role in this activation pathway. The Vav/PKCθ-mediated signals preferentially activated IκB kinase β. Vav and PKCθ were found to be constitutively associated in unstimulated T cells. Only the ligation of the costimulatory CD28 receptor, but not of the T cell receptor, resulted in the transient dissociation of the Vav-PKCθ complex. In contrast, T cell receptor/CD28 costimulation resulted in faster dissociation and slower reassociation kinetics.</p>
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Beschreibung:Online Resource
ISSN:1083-351X
DOI:10.1074/jbc.C000177200