کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2581689 | 1130201 | 2010 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
HTLV-1 Tax: Linking transformation, DNA damage and apoptotic T-cell death
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
CREBChk1HTLV-1 TaxATM kinaseFLICE inhibitory proteinATLPCNALTRHTLV-1FLIPataxia telangiectasia mutated kinaseAP-1EBNA-1SRFAPCNF-kBBESCHK2NER - DOWNHAM/TSP - HAM / TSPROS - ROSDNA damage - آسیبDNAanaphase promoting complex - آنافاز ترویج پیچیدهProliferating Cell Nuclear Antigen - آنتیژن هسته ای تکثیر سلولیcheckpoint kinase 1 - بازرسی کیناز 1checkpoint kinase 2 - بازرسی کیناز 2nucleotide excision repair - تعمیر مجدد نوکلئوتیدیbase excision repair - تعمیر پایه پایهLong terminal repeats - تکرار طولانی مدتTransformation - دگرگونیnuclear factor kappa B - فاکتور هسته ای کاپا BFLICE - فلیسTRAIL - قطارAdult T-cell leukemia - لوسمی T-cell بزرگسالانTNF-related apoptosis-inducing ligand - لیگاند ناشی از آپوپتوز مرتبط با TNFApoptotic cell death - مرگ سلولی آپوپتوزReactive oxygen intermediates - واکنش اکسیژن واسطهViral oncogenes - ویروس انکوژنcyclic AMP response element-binding protein - پروتئین اتصال دهنده عنصر Response Cyclic AMPactivator protein 1 - پروتئین فعال کننده 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The human T-cell leukemia virus type I (HTLV-1) is the causative agent of adult T-cell leukemia (ATL), an aggressive CD4-positive T-cell neoplasia. The HTLV-1 proto-oncogene Tax, a potent transcriptional activator of cellular and viral genes, is thought to play a pivotal role in the transforming properties of the virus by deregulating intracellular signaling pathways. During the course of HTLV-1 infection, the dysregulation of cell-cycle checkpoints and the suppression of DNA damage repair is tightly linked to the activity of the viral oncoprotein Tax. Tax activity is associated with production of reactive oxygen intermediates (ROS), chromosomal instability and DNA damage, apoptotic cell death and cellular transformation. Changes in the intracellular redox status induced by Tax promote DNA damage. Tax-mediated DNA damage is believed to be essential in initiating the transformation process by subjecting infected T cells to genetic changes that eventually promote the neoplastic state. Apoptosis and immune surveillance would then exert the necessary selection pressure for eliminating the majority of virally infected cells, while escape variants acquiring a mutator phenotype would constitute a subpopulation of genetically altered cells prone to neoplasia. While the potency of Tax-activity seems to be a determining factor for the observed effects, the cooperation of Tax with other viral proteins determines the fate and progression of HTLV-1-infected cells through DNA damage, apoptosis, survival and transformation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 188, Issue 2, 5 November 2010, Pages 359-365
Journal: Chemico-Biological Interactions - Volume 188, Issue 2, 5 November 2010, Pages 359-365
نویسندگان
Katerina Chlichlia, Khashayarsha Khazaie,