Abstract Apoptosis is a fundamental process that is required for the normal development and functioning of the immune system. It can be induced in different ways depending on cell type and acquired signal. Since the NF-κB transcription factor complex is believed to be involved in nitric oxide-induced apoptosis, the aim of this study was to investigate NF-κB and nitric oxide synthase (NOS) activity during dimethyl sulphoxide (DMSO)-dependent cell death of RPMI-8402 human pre-T cells. Our results show that NF-κB activation is associated with a significant up-regulation of NOS activity and induction of apoptosis. Furthermore, the inhibition and reversal of these effects by parthenolide treatment or DMSO removal indicate that these molecules are directly involved in the progression of cell death.

NF-κB and NOS may play a role in human RPMI-8402 cell apoptosis / Trubiani, O.; Salvolini, Eleonora; Vignini, Arianna; D'Arcangelo, C.; DI PRIMIO, Roberto; Mazzanti, Laura. - In: CELL BIOLOGY INTERNATIONAL. - ISSN 1065-6995. - 29:7(2005), pp. 529-536. [10.1016/j.cellbi.2005.03.007]

NF-κB and NOS may play a role in human RPMI-8402 cell apoptosis

SALVOLINI, Eleonora;VIGNINI, Arianna;DI PRIMIO, Roberto;MAZZANTI, LAURA
2005-01-01

Abstract

Abstract Apoptosis is a fundamental process that is required for the normal development and functioning of the immune system. It can be induced in different ways depending on cell type and acquired signal. Since the NF-κB transcription factor complex is believed to be involved in nitric oxide-induced apoptosis, the aim of this study was to investigate NF-κB and nitric oxide synthase (NOS) activity during dimethyl sulphoxide (DMSO)-dependent cell death of RPMI-8402 human pre-T cells. Our results show that NF-κB activation is associated with a significant up-regulation of NOS activity and induction of apoptosis. Furthermore, the inhibition and reversal of these effects by parthenolide treatment or DMSO removal indicate that these molecules are directly involved in the progression of cell death.
2005
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11566/33951
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