کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8499413 | 1553625 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The GRIM-19 plays a vital role in shrimps' responses to Vibrio alginolyticus
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
علوم آبزیان
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چکیده انگلیسی
GRIM-19 (gene associated with retinoid-interferon-induced mortality 19), a novel cell death regulatory gene, plays important roles in cell apoptosis, mitochondrial respiratory chain and immune response. It has been reported to interact physically with STAT3 and inhibit STAT3-dependent signal transduction. In this study, a new GRIM-19 gene, which is a 789-bp gene encoding a 149 amino acids protein, is identified and characterized from Litopenaeus vannamei. The tissue distribution patterns showed that LvGRIM-19 was widely expressed in all examined tissues, with the highest expression in muscle. Quantitative real-time PCR revealed that LvGRIM-19 was down-regulated in hepatopancreas after infection with the Vibrio alginolyticus. Knockdown of LvGRIM-19 by RNA interference resulted in a lower mortality of L. vannamei under V. alginolyticus infection, as well as an enhancement in the protein expression of STAT gene and JAK gene. V. alginolyticus infection caused an increase apoptotic cell ratio and ROS production of L. vannamei, while LvGRIM-19 silenced shrimps showed significantly lower than GFP group. Our results suggest that the GRIM-19 plays a vital role in shrimps' responses to V. alginolyticus. Interferenced LvGRIM-19 treatment during V. alginolyticus infection could increase 12 h survival rate, which might indicated that LvGRIM-19 is closely related to death of shrimps.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Fish & Shellfish Immunology - Volume 49, February 2016, Pages 34-44
Journal: Fish & Shellfish Immunology - Volume 49, February 2016, Pages 34-44
نویسندگان
Ting Peng, Mei-mei Gu, Chang-sheng Zhao, Wei-na Wang, Ming-zhu Huang, Chen-ying Xie, Yu-chao Xiao, Gui-Hong Cha, Yuan Liu,