Tec kinase stimulates cell survival in transfected Hek293T cells and is regulated by the anti-apoptotic growth factor IGF-I in human neutrophils.

Autor: Himpe E; Center for Neurosciences, Department of Pharmacology, Vrije Universiteit Brussel, Brussels, Belgium. Ehimpe@gmail.com, Abdul Rahim SA, Verdood P, Mano H, Kooijman R
Jazyk: angličtina
Zdroj: Cellular signalling [Cell Signal] 2013 Mar; Vol. 25 (3), pp. 666-73. Date of Electronic Publication: 2012 Dec 19.
DOI: 10.1016/j.cellsig.2012.12.002
Abstrakt: Objective: Previously, we showed that the phosphatidylinositol-3 kinase (PI(3)K) pathway mediates the anti-apoptotic effects of IGF-I in human neutrophils independently of its down-stream target Akt. In this study, we investigated whether IGF-I regulates Tec kinase, an alternative down-stream target of PI(3)K, in neutrophils and whether this molecule is able to affect apoptosis.
Design: We investigated the translocation of Tec kinases in neutrophils after stimulation with IGF-I. Furthermore, we transiently and stably transfected Hek293T cells with constructs expressing different forms of Tec kinase and measured the level of cell survival and apoptosis/necrosis through trypan blue exclusion test and Annexin-V/propidium iodide labelling, respectively.
Results: We show that IGF-I stimulates the translocation of Tec kinase to the membrane in neutrophils in a PI(3)K dependent matter. Overexpression of Tec kinase augments cell survival by inhibition of necrosis. The pro-survival effect is attenuated by the deletion of the kinase domain but not by inactivation of this domain by a single amino acid substitution.
Conclusion: Tec kinase can act as a prosurvival factor and is regulated by IGF-I in human neutrophils through PI(3)K activation.
(Copyright © 2012 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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