کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5905871 | 1159942 | 2014 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Arsenic programmes cellular genomic-immunity through miR-2909 RNomics
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کلمات کلیدی
APOBEC3GRIG1IFNβIRF3KLF4PBMCsFCSNFκB - NFKBArsenic - آرسنیکInterferon beta - اینترفرون بتاGene regulation - تنظیم ژنfoetal calf serum - سرم گوساله جنینperipheral blood mononuclear cells - سلول های تک هسته ای خون محیطیCyld - سیلدCylindromatosis - سیلیندروماتوزInterferon regulatory factor 3 - عامل تنظیمی اینترفرون 3nuclear factor kappa B - فاکتور هسته ای کاپا BMicroRNA - میکرو RNA MiRNA - میکروRNA، ریزآرانای، miRNAretinoic acid-inducible gene 1 - ژن القاء شده اسید رتینوئیک 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
ژنتیک
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
It is widely recognized that human cells are equipped with innate antiviral-RNA armour involving the production of type I interferons and APOBEC3G (apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3G) gene-product. Although arsenic has been shown to have paradoxical effect on one arm of this armour involving APOBEC3G, the exact molecular mechanism of its action in this regard is far from clear. The present study, addressed to explore as to how arsenic programmes this innate antiviral-RNA cellular-sensing pathway, clearly revealed that arsenic programmes this innate cellular antiviral genomic response through its inherent capacity to initiate cellular miR-2909 RNomics pathway, involving not only the modulation of APOBEC3G gene but also KLF4 (Kruppel-like factor 4) dependent regulation of gene coding for IKBKε (Inhibitor of nuclear factor kappa-B kinase subunit epsilon) which in turn modulates RIG-I (retinoic acid-inducible gene 1) pathway responsible for the production of IFNβ (interferon beta) through restriction of CYLD (Cylindromatosis) deubiqutinating activity. This restricted inhibitory enzyme activity of CYLD upon NFkB (nuclear factor kappa-light-chain-enhancer of activated B cells) also ensures sustained expression of miR-2909. Our results for the first time show that cellular miR-2909 RNomics may constitute an innate genomic armour to promote as well as restrict retroviral infection.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gene - Volume 536, Issue 2, 25 February 2014, Pages 326-331
Journal: Gene - Volume 536, Issue 2, 25 February 2014, Pages 326-331
نویسندگان
Deepak Kaul, S. Sharma, M. Sharma, M. Arora, Mansi Arora,