A CgIFNLP receptor from Crassostrea gigas and its activation of the related genes in human JAK/STAT signaling pathway
Interferon is a highly pleiotropic cytokine, once binding to its receptors, can activate JAK kinases and STAT transcription factors to initiate the transcription of genes downstream from interferon-stimulated response elements. In the present study, a cytokine receptor-like 3 molecule was selected a...
Published in: | Developmental & Comparative Immunology |
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Main Authors: | , , , , , , |
Format: | Article in Journal/Newspaper |
Language: | English |
Published: |
2016
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Subjects: | |
Online Access: | http://ir.qdio.ac.cn/handle/337002/135895 https://doi.org/10.1016/j.dci.2016.06.010 |
Summary: | Interferon is a highly pleiotropic cytokine, once binding to its receptors, can activate JAK kinases and STAT transcription factors to initiate the transcription of genes downstream from interferon-stimulated response elements. In the present study, a cytokine receptor-like 3 molecule was selected and cloned from oyster Crassostrea gigas, which contained a fibronectin type III domain (designed CgIFNR-3). The expression pattern of CgIFNR-3 mRNA was detected in all the tested tissues including mantle, gills, hepatopancreas, muscle, and hemocytes, with the highest expression level in hemocytes. After poly (I: C) stimulation, the expression level of CgIFNR-3 in hemocytes was observed to significantly increase at 3 h (13.06-fold, p < 0.01). CgIFNR-3 was indicated to interact with CgIFNLP by in vitro GST pull-down assay, and to activate the expression of transcription factors including ISRE, STAT3 and GAS, in human Janus kinase signal transducer and activator of transcription (JAK/STAT) pathway after co-transfection in HEK-293T cells in the reporter luciferase activity assay. These results suggested that CgIFNR-3 could bind to CgIFNLP as an interferon receptor and participate in the activation of JAK/STAT pathway in human, which will benefit for intensive studies of interferon signaling pathway in mollusc. (C) 2016 Elsevier Ltd. All rights reserved. |
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