کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2132260 1547707 2008 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Both IKKα and IKKβ are implicated in the arsenite-induced AP-1 transactivation correlating with cell apoptosis through NF-κB activity-independent manner
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی تحقیقات سرطان
پیش نمایش صفحه اول مقاله
Both IKKα and IKKβ are implicated in the arsenite-induced AP-1 transactivation correlating with cell apoptosis through NF-κB activity-independent manner
چکیده انگلیسی

Arsenite has been well-proved to act as both an environmental carcinogen as well as a tumor therapeutic agent. AP-1 is one of the transcription factors that can be induced upon arsenite stimulation. However, the study on the mechanism and the function of the arsenite-induced AP-1 transactivation remains far complete. Here we demonstrated that high dose of arsenite induced apoptotic response in mouse fibroblasts correlating with AP-1 transactivation, which events were mediated by both IKKα and IKKβ, two major protein kinases responsible for NF-κB activation. In addition, the regulatory effect of IKKs on the arsenite-induced AP-1 activation was delivered by sequential induction of GADD45α expression and the activation of MAPKK (MKK3/4/6) and MAPK (JNK and p38K)-dependent pathways. We further provided evidence that p50, but not p65 subunit of NF-κB, was involved in GADD45α induction and the subsequent MAPKK/MAPK/AP-1 activation under arsenite exposure, while functional NF-κB induced by arsenite stimulation consisted of p65 but not of p50 subunit. Therefore, we concluded that both IKKα and IKKβ can mediate arsenite-induced AP-1 transactivation through NF-κB activity-independent manner.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 314, Issues 11–12, 1–15 July 2008, Pages 2187–2198
نویسندگان
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