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

• Verfasst von: Dienz, Oliver [VerfasserIn]
• Verfasst von: Dröge, Wulf [VerfasserIn]
• Titel: Synergistica activation of NF-κB by functional cooperation between Vav and PKCθ in T lymphocytes
• Verf.angabe: Oliver Dienz, Steffen P. Hehner, Wulf Dröge, and M. Lienhard Schmitz
• E-Jahr: 2000
• Jahr: June 21, 2000
• Umfang: 5 S.
• Fussnoten: Gesehen am 03.02.2021
• Titel Quelle: Enthalten in: The journal of biological chemistry
• Ort Quelle: Bethesda, Md. : Soc., 1905
• Jahr Quelle: 2000
• Band/Heft Quelle: 275(2000), 32, Seite 24547-24551
• ISSN Quelle: 1083-351X
• DOI: doi:10.1074/jbc.C000177200
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1747220086

Abstract

<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>