دورية أكاديمية

Differential upregulation of human 2′5′ OAS genes on systemic sclerosis: Detection of increased basal levels of OASL and OAS2 genes through a qPCR based assay.

التفاصيل البيبلوغرافية
العنوان: Differential upregulation of human 2′5′ OAS genes on systemic sclerosis: Detection of increased basal levels of OASL and OAS2 genes through a qPCR based assay.
المؤلفون: de Freitas Almeida, Gabriel Magno, Oliveira, Danilo Bretas de, Botelho, Lucas Moreira, Silva, Ludmila Karen dos Santos, Guedes, Antônio Carlos Martins, Santos, Flávia Patrícia Sena Teixeira, Bonjardim, Cláudio Antônio, Ferreira, Paulo César Peregrino, Kroon, Erna Geessien
المصدر: Autoimmunity; Mar2014, Vol. 47 Issue 2, p119-126, 8p
مصطلحات موضوعية: SCLERODERMA (Disease), HUMAN genes, OLIGOADENYLATE synthetase, AUTOIMMUNITY, HOMEOSTASIS, INTERFERONS, PATIENTS
مستخلص: 2′5′OAS are template-independent RNA polymerases with antiviral activity and important to homeostasis maintenance. Here we have developed quantitative PCR (qPCR) reactions for the detection of each individual 2′5′ OAS human gene and used them to evaluate these gene levels in systemic sclerosis patients cells. The method was efficient for quantification of 2′5′ OAS genes on human cells after interferon (IFN) treatment, and revealed that primary cells from patients with systemic sclerosis have increased basal levels of OASL and OAS2 genes. When treated, patients cells are able to induce all four 2′5′ OAS genes. Our hypothesis is that abnormally circulating type I IFNs on the disease could be establishing a desensitized state on patients cells, making them refractory to subsequent IFN doses, and that OASL and OAS2 genes upregulation may be due to an IFN-independent stimulus. Further characterizing the biological activities of these genes, their induction pathways and their regulatory functions can lead to better understanding of systemic sclerosis molecular mechanisms and of their biological activities. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:08916934
DOI:10.3109/08916934.2013.866102