کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
1937403 1050715 2007 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Epstein-Barr virus-encoded LMP1 promotes cisplatin-induced caspase activation through JNK and NF-κB signaling pathways
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Epstein-Barr virus-encoded LMP1 promotes cisplatin-induced caspase activation through JNK and NF-κB signaling pathways
چکیده انگلیسی

Our previous studies have shown that Epstein-Barr virus (EBV)-encoded latent membrane protein 1 (LMP1) potentiates chemotherapeutic agent-induced apoptosis in human cell lines of epithelial origin: cervical carcinoma-derived HeLa cells and nasopharyngeal carcinoma-derived TW03 cells. LMP1 acted upstream of caspase-dependent mitochondrial perturbation, and the effect was mapped to the C-terminal signaling domain of LMP1, designated CTAR2. CTAR2 is known to engage the c-Jun N-terminal kinase (JNK) and NF-κB pathways, and we show here that SP600125, a selective JNK inhibitor, suppresses LMP1 potentiation of cisplatin-induced mitochondrial damage and caspase activation in HeLa cells. Moreover, the potentiation of cisplatin-triggered caspase activation was blocked by Bay11-7082, a potent inhibitor of NF-κB. Similar results were obtained when a dominant negative form of IκB, a specific repressor of NF-κB, was co-expressed with LMP1. The current data support the notion that LMP1 modifies stress-induced apoptosis in epithelial cells through molecular interactions downstream of its C-terminal signaling domain.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 360, Issue 1, 17 August 2007, Pages 263–268
نویسندگان
, , , , ,