کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8326266 | 1539965 | 2008 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Ku, Artemis, and ataxia-telangiectasia-mutated: Signalling networks in DNA damage
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کلمات کلیدی
DSBsDNA-PKcsDNA-PKAtaxia-telangiectasiaCHK2H2AXMRE11XRCC4NHEJMre11/Rad50/Nbs1ATRNBS1ATR-interacting proteinCDKmeiotic recombination 11Mdm2 - MDM2PI-3-kinase - PI-3-کینازROS - ROSArtemis - آرتمیسDNA damage - آسیبDNAATM - خودپردازATRIP - سفرNijmegen breakage syndrome 1 - سندرم شکستن نیهمگن 1double-strand breaks - شکست دو ردیفnon-homologous end joining - عدم پیوستن انتهای غیر همولوگphosphoinositide-3-kinase - فسفونیوییدید-3-کینازMouse double minute 2 - ماوس دو دقیقه 2Homologous recombination - نوترکیبی همولوگHistone H2AX - هیستون H2AXDNA-dependent protein kinase - وابسته به پروتئین کیناز وابسته به DNAcyclin-dependent kinase - کییناز وابسته به سیکلینReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Cell death linked to DNA damage has been implicated in various diseases caused by environmental stress and infection. Severe DNA damage, which is beyond the capacity of the DNA repair proteins, triggers apoptosis. Accumulation of DNA damage has been proposed to be a principal mechanism of infection, inflammation, cancer, and aging. The most deleterious form of DNA damage is double-strand breaks (DSBs), where ataxia-telangiectasia-mutated (ATM) is the main transducer of the double-strand DNA break signal. Once the DNA is damaged, the DNA repair protein Ku70/80 translocates into the nucleus, a process which may be mediated by ataxia-telangiectasia-mutated, a member of the phosphoinositide-3-kinase-like family. The function and stability of Artemis may also be regulated by ataxia-telangiectasia-mutated through its phosphorylation upon the occurrence of DNA damage. Interestingly, both Artemis and Ku70/80 are substrates of DNA-dependent protein kinase (DNA-PK), another member of the phosphoinositide-3-kinase-like family. In this review, we show how Ku and Artemis function in the DNA damage response and the ataxia-telangiectasia-mutated signaling pathway and discuss potential applications of agents targeting these DNA damage response molecules in the treatment of inflammation and cancer.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 40, Issue 4, 2008, Pages 598-603
Journal: The International Journal of Biochemistry & Cell Biology - Volume 40, Issue 4, 2008, Pages 598-603
نویسندگان
Tomohiro Morio, Hyeyoung Kim,