کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2428965 1106464 2015 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Two myeloid differentiation factor 88 (MyD88) isoforms identified in ducks
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شناسی تکاملی
پیش نمایش صفحه اول مقاله
Two myeloid differentiation factor 88 (MyD88) isoforms identified in ducks
چکیده انگلیسی


• Two myeloid differentiation factor 88 isoforms (DuMyD88-X1 and DuMyD88-X2) were identified in ducks.
• The expression of the two MyD88 isoforms showed different expression patterns in the healthy and NDV infected duck tissues.
• Overexpression of DuMyD88-X1 and DuMyD88-X2 induced the activation of NF-κB and IL-6.
• DuMyD88-X1 more strongly activated NF-κB signal pathway compared to DuMyD88-X2.

MyD88 is an adaptor protein involved in the interleukin-1 receptor-induced and Toll-like receptor (TLR)-induced activation of nuclear factor-κB (NF-κB). In this study, we identified two isoforms of MyD88 gene, designated DuMyD88-X1 and DuMyD88-X2, from duck cells. Both variants were determined to have a death domain at the N-terminal and a Toll/IL-1R (TIR) domain at the C-terminal; however, the TIR domain of DuMyD88-X2 was incomplete and was 81 amino acids shorter than DuMyD88-X1. Quantitative real-time reverse transcription PCR revealed broad expression of both MyD88s. During Newcastle disease virus (NDV) challenge experiments, expression of the two genes increased significantly, with DuMyD88-X1 having a larger amplitude and longer duration. Overexpression of DuMyD88-X1 and DuMyD88-X2 induced the activation of NF-κB and IL-6 in vitro, suggesting that DuMyD88-X1 and DuMyD88-X2 may be important in the innate immune response. The results verify the existence of a MyD88-dependent signaling pathway in ducks and contribute to understanding the potential role of MyD88s in the innate immune response.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Developmental & Comparative Immunology - Volume 52, Issue 2, October 2015, Pages 144–154
نویسندگان
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