Murine erythroleukemia cells (Friend) respond to ionizing radiation with the activation and nuclear translocation of p85alpha subunit of phosphatidylinositol-3-kinase (PI-3-kinase) which mediates the downstream activation and nuclear translocation of atypical Protein kinase C zeta (PKC zeta). This event occurs mainly upon high dose of ionizing radiation (15 Gy) and is concomitant to an increase in BrdU incorporation, which probably accounts for a predominant repair DNA synthesis. Following treatment with wortmannin, a relatively specific inhibitor of PI-3-kinase, both an increased number of apoptotic cells and the inhibition of protein kinase C zeta translocation were detected. Altogether the evidence suggests a potential role of the PI-3-kinase/PKC zeta pathway in protecting Friend cells from ionizing radiation-induced apoptosis offering PKC zeta for consideration as possible target of pharmacological treatments.

Cataldi, A., Di Pietro, R., Centurione, L., Rapino, M., Santavenere, E., Garaci, F., et al. (2003). Engagement of PI-3-kinase mediated Protein kinase C zeta activation in protecting Friend cells from ionizing radiation-induced apoptosis. INTERNATIONAL JOURNAL OF ONCOLOGY, 22(1), 129-135.

Engagement of PI-3-kinase mediated Protein kinase C zeta activation in protecting Friend cells from ionizing radiation-induced apoptosis

GARACI, FRANCESCO;
2003-01-01

Abstract

Murine erythroleukemia cells (Friend) respond to ionizing radiation with the activation and nuclear translocation of p85alpha subunit of phosphatidylinositol-3-kinase (PI-3-kinase) which mediates the downstream activation and nuclear translocation of atypical Protein kinase C zeta (PKC zeta). This event occurs mainly upon high dose of ionizing radiation (15 Gy) and is concomitant to an increase in BrdU incorporation, which probably accounts for a predominant repair DNA synthesis. Following treatment with wortmannin, a relatively specific inhibitor of PI-3-kinase, both an increased number of apoptotic cells and the inhibition of protein kinase C zeta translocation were detected. Altogether the evidence suggests a potential role of the PI-3-kinase/PKC zeta pathway in protecting Friend cells from ionizing radiation-induced apoptosis offering PKC zeta for consideration as possible target of pharmacological treatments.
2003
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/36 - DIAGNOSTICA PER IMMAGINI E RADIOTERAPIA
English
Con Impact Factor ISI
PI-3-kinase; protein kinase C zeta; apoptosis; ionizing radiation
phosphatidylinositol 3-kinase activity; phosphoinositide 3-kinase; inositol lipids; tyrosine kinase; nuclei; tumor; delta; differentiation; diacylglycerol; translocation
Cataldi, A., Di Pietro, R., Centurione, L., Rapino, M., Santavenere, E., Garaci, F., et al. (2003). Engagement of PI-3-kinase mediated Protein kinase C zeta activation in protecting Friend cells from ionizing radiation-induced apoptosis. INTERNATIONAL JOURNAL OF ONCOLOGY, 22(1), 129-135.
Cataldi, A; Di Pietro, R; Centurione, L; Rapino, M; Santavenere, E; Garaci, F; Cocco, L; Giuliani Piccari, G; Rana, R
Articolo su rivista
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/70307
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