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Oxidative stress attenuates Fas-mediated apoptosis in Jurkat T cell line through Bfl-1 induction
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Heejung | - |
dc.contributor.author | Kim, Yong-Nyun | - |
dc.contributor.author | Kim, Hyungsoo | - |
dc.contributor.author | Kim, Chul-Woo | - |
dc.date.accessioned | 2009-09-22T13:31:17Z | - |
dc.date.available | 2009-09-22T13:31:17Z | - |
dc.date.issued | 2004-12-14 | - |
dc.identifier.citation | Oncogene 24: 1252-1261 | en |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | https://hdl.handle.net/10371/9686 | - |
dc.description.abstract | Many types of mammalian cells produce ROS in response to many different stimuli to modulate a number of cellular functions, including apoptosis. However, the correlation between ROS and apoptosis remains controversial, and the mechanisms whereby ROS-induced signals are propagated to critical downstream targets remain largely undefined. Here, we demonstrate that hydrogen peroxide (H2O2) upregulates the expression of Bfl-1, an antiapoptotic member of the Bcl-2 family, and that this is responsible for the antiapoptotic activity of ROS. When Jurkat, human leukemic T cells, were pretreated with 100 microM H2O2 and then treated with anti-Fas antibody, apoptosis was impaired without change of cell surface Fas expression. An investigation of the expression patterns of Bcl-2 family genes revealed that H2O2 treatment induced Bfl-1 gene expression, but left other genes unchanged, and this Bfl-1 expression and H2O2 -induced antiapoptotic effect was inhibited by antioxidants or NF-kappaB inhibitor. In addition, an electromobility shift assay revealed that the p65/p50 subunits of NF-kappaB activated by H2O2 bound to a bfl-1 promoter. Neither the induction of Bfl-1 nor the antiapoptotic effect of H2O2 was detected in Bfl-1-knockdown Jurkat cell line containing Bfl-1 antisense (Bfl-1AS). These data indicate that oxidative stress induces the expression of Bfl-1 via NF-kappaB activation, and this early-response gene protects cells from Fas-mediated apoptosis. This may be a cellular survival mechanism of cells exposed to phagocytes-derived ROS. | en |
dc.description.sponsorship | This work was supported by the Korea Science & Engineering
Foundation (KOSEF) through the Tumor Immunity Medical Research Center at Seoul National University College of Medicine. | en |
dc.language.iso | en | - |
dc.publisher | Nature Publishing Group | en |
dc.subject | hydrogen peroxide | en |
dc.subject | apoptosis | en |
dc.subject | Bfl-1 | en |
dc.subject | NF-kappaB | en |
dc.title | Oxidative stress attenuates Fas-mediated apoptosis in Jurkat T cell line through Bfl-1 induction | en |
dc.type | Article | en |
dc.contributor.AlternativeAuthor | 김희정 | - |
dc.contributor.AlternativeAuthor | 김용년 | - |
dc.contributor.AlternativeAuthor | 김형수 | - |
dc.contributor.AlternativeAuthor | 김철우 | - |
dc.identifier.doi | 10.1038/sj.onc.1208282 | - |
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