کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278496 | 1295819 | 2007 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The case for 8,5â²-cyclopurine-2â²-deoxynucleosides as endogenous DNA lesions that cause neurodegeneration in xeroderma pigmentosum
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کلمات کلیدی
Jnk8-oxo-dGBERMAODCsRNA polymerase II - آرانای پلیمراز II GC-MS - کروماتوگرافی گازی-طیف سنج جرمی8-oxo-2′-deoxyguanosine - 8-اکسو-2'-دگزسی گوانوزینc-Jun N-terminal kinase - C-Jun N-terminal kinaseNER - DOWNxeroderma pigmentosum - pigmentosum xerodermaUltraviolet - اشعه فرابنفشParkinson’s disease - بیماری پارکینسونDNA repair - ترمیم DNAnucleotide excision repair - تعمیر مجدد نوکلئوتیدیbase excision repair - تعمیر پایه پایهtyrosine hydroxylase - تیروزین هیدروکسیلازDopamine - دوپامینTranscription - رونویسیCockayne syndrome - سکته Cockaynegas chromatography–mass spectrometry - طیف سنجی جرم کروماتوگرافی گازCSF - مایع مغزی نخاعیCerebrospinal fluid - مایع مغزی نخاعیPdG - مدیر عامل شرکتmonoamine oxidase - مونوآمین اکسیدازها homovanillic acid - هومووانیلیک اسیدPol II - پل دومHVA - چه
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Patients with the genetic disease xeroderma pigmentosum (XP) lack the capacity to carry out a specific type of DNA repair process called nucleotide excision repair (NER). The NER pathway plays a critical role in the repair of DNA damage resulting from ultraviolet (UV) radiation. A subset of XP patients develops a profound neurodegenerative condition known as XP neurological disease. Robbins and colleagues [Andrews A, Barrett S, Robbins J (1978) Xeroderma pigmentosum neurological abnormalities correlate with the colony forming ability after ultraviolet irradiation. Proc Natl Acad Sci U S A 75:1984-1988] hypothesized that since UV light cannot reach into the human brain, XP neurological disease results from some form of endogenous DNA damage that is normally repaired by the NER pathway. In the absence of NER, the damage accumulates, causing neuronal death by blocking transcription. In this manuscript, I consider the evidence that a particular class of oxidative DNA lesions, the 8,5â²-cyclopurine-2â²-deoxynucleosides, fulfills many of the criteria expected of neurodegenerative DNA lesions in XP. Specifically, these lesions are chemically stable, endogenous DNA lesions that are repaired by the NER pathway but not by any other known process, and strongly block transcription by RNA polymerase II in cells from XP patients. A similar set of criteria might be used to evaluate other candidate DNA lesions responsible for neurological diseases resulting from defects in other DNA repair mechanisms as well.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 145, Issue 4, 14 April 2007, Pages 1407-1417
Journal: Neuroscience - Volume 145, Issue 4, 14 April 2007, Pages 1407-1417
نویسندگان
P.J. Brooks,