کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1985091 | 1539953 | 2009 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Regulation of poly(ADP-ribose) polymerase-1 functions by leukocyte elastase inhibitor/LEI-derived DNase II during caspase-independent apoptosis
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کلمات کلیدی
MNNGBHKPCDLEIPARPpoly-ADP-riboseCaspase-independentPoly-ADP-ribose-polymeraseMEFPARP-1L-DNase IIDNAse - DNAaseN-methyl-N′-nitro-N-nitrosoguanidine - N-methyl-N'-nitro-N-nitrosoguanidineAIF - آیفونbaby hamster kidney - بچه هامستر کلیهPar - توسطApoptosis - خزان یاختهایCAD - طراحی به کمک رایانه یا کَدapoptosis-inducing factor - عامل القاء آپوپتوزProgrammed cell death - مرگ برنامهریزی شده یاختهLeukocyte elastase inhibitor - مهار کننده الاستاز لکوسیتیmouse embryonic fibroblasts - موش فیبروبلاست جنینیProtease - پروتئازcaspase-activated DNase - کاسپاز فعال DNase
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Poly(ADP-ribose) polymerase-1 (PARP-1) is an important regulator of apoptosis. Its over-activation at the onset of apoptosis can inhibit the action of apoptotic endonucleases like caspase-activated DNase and DNAS1L3. Therefore, controlled PARP-1 proteolysis during caspase-dependent apoptosis is considered essential to promote DNA degradation. Yet, little is known about the interplay of PARP-1 and endonucleases that operate during caspase-independent cell death. Here we show that in the long-term cultured HeLa cells which undergo caspase-independent death, PARP-1 co-immunoprecipitates with leukocyte elastase inhibitor-derived DNase II (L-DNase II), an acid DNase implicated in this death pathway and activated by serine proteases. Our results indicate that, despite having putative poly(ADP-ribose)-acceptor sites, LEI/L-DNase II is neither significantly poly(ADP-ribosyl)ated nor inhibited by PARP-1 during caspase-independent apoptosis. Unexpectedly, caspase-independent apoptosis induced by hexa-methylene amiloride, LEI/L-DNase II can activate PARP-1 and promote its auto-poly(ADP-ribosyl)ation, thus inhibiting PARP-1 activity. Moreover, overexpression of LEI blocks the pro-survival effect of PARP-1 in this model of cell death. Our results provide the original evidence for a new mechanism of PARP-1 activity regulation in the caspase-independent death pathway involving LEI/L-DNase II.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 41, Issue 5, May 2009, Pages 1046-1054
Journal: The International Journal of Biochemistry & Cell Biology - Volume 41, Issue 5, May 2009, Pages 1046-1054
نویسندگان
C. Leprêtre, A.I. Scovassi, G.M. Shah, A. Torriglia,