کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10816528 | 1058577 | 2005 | 15 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Daxx overexpression in T-lymphoblastic Jurkat cells enhances caspase-dependent death receptor- and drug-induced apoptosis in distinct ways
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کلمات کلیدی
JC-1poly-(ADP-ribose)-polymeraseXIAPDAXXPARPBcl-2FASPAR-4 - BY-4cIAP - ciapcellular Inhibitor of Apoptosis - بازدارنده سلولی آپوپتوزBax - باکسApoptosis - خزان یاختهایDoxorubicin - دوکسوروبیسینTRAIL - قطارX-linked inhibitor of apoptosis - مهارکننده آپوپتوز X مرتبط با آنdeath-associated protein - پروتئین مرتبط با مرگCaspases - کاسپاز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The role of Daxx, in particular, its ability to promote or hinder apoptosis, still remains controversial. In order to elucidate the functional relevance of Daxx in apoptosis signaling of malignant lymphocytes, Jurkat T-cells were stably transfected with a Daxx-expressing vector or with the respective Daxx-negative control vector. We thus demonstrate that ectopic expression of Daxx substantially increases the rate of apoptosis upon incubation with death receptor agonists such as Fas and TRAIL as well as upon incubation with the cytotoxic drug doxorubicin (DOX). Analysis of the molecular changes induced in the extrinsic and intrinsic apoptosis pathways reveals that augmentation of apoptosis by Daxx overexpression is conveyed by distinctly different mechanisms. Although enforced apoptosis caused by ectopic Daxx expression is caspase-dependent in both cases, major differences between Fas/TRAIL-induced apoptosis and doxorubicin-induced apoptosis are observed in expression patterns of X-linked inhibitor of apoptosis (XIAP), p53, Bid, ZIP kinase, and prostate apoptosis response gene 4 (Par-4). Moreover, we could show that addition of a CD95 blocking antibody to the clones treated with doxorubicin was able to increase apoptosis as compared to doxorubicin treatment alone and was accompanied by an enhancement of the mitochondrial branch of apoptosis. In conclusion, we here outline the major molecular mechanisms underlying the apoptosis-promoting effect of Daxx in neoplastic lymphocytes and demonstrate fundamental molecular differences elicited by the overexpression of Daxx in the extrinsic and intrinsic signaling pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 17, Issue 5, May 2005, Pages 581-595
Journal: Cellular Signalling - Volume 17, Issue 5, May 2005, Pages 581-595
نویسندگان
Simone Boehrer, Daniel Nowak, Simone Hochmuth, Soo-Zin Kim, Bettina Trepohl, Amina Afkir, Dieter Hoelzer, Paris S. Mitrou, Eckhart Weidmann, Kai Uwe Chow,