کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10143161 | 1646154 | 2019 | 17 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Identification and characterization of the interferon-γ-inducible lysosomal thiol reductase gene in Chinese soft-shelled turtle, Pelodiscus sinensis
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی تکاملی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
The reduction of disulfide bonds of exogenous antigens is crucial to the MHC-II class antigen processing and presenting pathway and is catalysed by interferon-γ-inducible lysosomal thiol reductase (GILT). In this study, a reptile GILT gene from Chinese soft-shelled turtle, Pelodiscus sinensis (PsGILT), was identified. The full-length cDNA of PsGILT is 1631 nucleotides (nt), including a 5â²-untranslated region (UTR) of 3â¯nt, a 3â²-UTR of 860â¯nt and an open reading frame (ORF) of 768â¯nt encoding 255 amino acids (aa). The conserved features in known GILTs, such as signal peptide, CXXC motif, GILT signature sequence, N-glycosylation site and conserved cysteines, were all found in the putative PsGILT protein. Genomic analysis revealed that PsGILT kept the “7 exons and 6 introns” structure of vertebrate GILT genes. PsGILT was expressed in all examined organs/tissues and was mainly expressed in spleen and blood. Increased mRNA expression levels of PsIFN-γ and PsGILT in PBLs were observed after induction with LPS, PolyI:C and recombinant IFN-γ (rIFN-γ). We also tested the reductase activity of rGILT in vitro and found that it could reduce intact human IgG into H chains and L chains. These above results implied that PsGILT may play an important role in resisting bacterial and viral infections, like other vertebrate GILTs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Developmental & Comparative Immunology - Volume 90, January 2019, Pages 55-59
Journal: Developmental & Comparative Immunology - Volume 90, January 2019, Pages 55-59
نویسندگان
Jianping Fu, Shannan Chen, Xin Zhao, Zhang Luo, Pengfei Zou, Yi Liu,