کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2146818 | 1548374 | 2010 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Differential regulation of caspase-9 by ionizing radiation- and UV-induced apoptotic pathways in thymic cells
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کلمات کلیدی
Bcl-xLDISCBcl-2CBBAPAf-1DAPI4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولBH3 Interacting Domain Death Agonist - BH3 تعامل دامنه آگونیست مرگBSA - BSACoomassie Brilliant Blue - Coomassie درخشان آبیbovine serum albumin - آلبومین سرم گاوApoptosome - آپوپتوزومionizing radiation - تابش یوننده یا پرتوهای یونیزانNSCLC - سرطان ریوی غیر سلول کوچکB-cell lymphoma 2 - لنفوم سلول B 2BID - پیشنهادdeath-inducing signaling complex - پیچیدگی سیگنالینگ ناشی از مرگnon-small cell lung carcinoma - کارسینوم ریه سلول غیر سلولیCaspases - کاسپاز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
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چکیده انگلیسی
In mouse thymic lymphoma 3SB cells bearing wild type p53, ionizing radiation (IR) and UV light are potent triggers of caspase-3-dependent apoptosis. Although cytochrome c was released from mitochondria as expected, caspase-9 activation was not observed in UV-exposed cells. Laser scanning confocal microscopy analysis showed that caspase-9 is localized in an unusual punctuated pattern in UV-induced apoptotic cells. In agreement with differences in the status of caspase-9 activation between IR and UV, subcellular protein fractionation experiments showed that pro-apoptotic apoptosis protease-activating factor 1 (Apaf-1), normally a part of the apoptosome assembled in response to the release of cytochrome c from mitochondria, and B-cell lymphoma extra long (Bcl-xL), an inhibitor of the change in mitochondrial membrane permeability, were redistributed by the IR-exposure but not by the UV-exposure. Instead of the sequestration of the capase-9/apoptosome activation in UV-induced apoptotic cells, the extrinsic apoptotic signaling generated by caspase-8 activation and consequent activation of B-cell lymphoma extra long (Bid) to release cytochrome c from mitochondria was observed. Thus, the post-mitochondrial apoptotic pathway downstream of cytochrome c release cannot operate the apoptosome function in UV-induced apoptosis in thymic 3SB cells. The intracellular redistribution and sequestration of apoptosis-related proteins upon mitochondrion-based apoptotic signaling was identified as a novel cellular mechanism to respond to DNA damage in an agent type-specific manner. This finding suggests that the kind of the critical ultimate apoptosis-inducing DNA lesion complex form resulting from the agent-specific DNA damage responses is important to determine which of apoptosis signals would be activated.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 688, Issues 1â2, 1 June 2010, Pages 78-87
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 688, Issues 1â2, 1 June 2010, Pages 78-87
نویسندگان
Mayumi Okamoto, Satomi Koga, Masaaki Tatsuka,