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Induction of inosine containing mRNA during the inflammatory stress in C57BL/6 mouse

机译:在C57BL / 6小鼠炎症应激中诱导含肌苷的mRNA表达。

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摘要

A-to-I RNA editing is a recently discovered process of post-transcription modification of pre-mRNA by adenosine deamination that results in the production of proteins not inherent in the genome. The present study aimed to identify a role for A-to-I RNA editing in the acute inflammation. It was found that A-to-I edtiting activities of RNA edi-tases, ADARs, were upregulated in lung, spleen, thymus and lymph node of mouse during endotoxin stimulation. Importantly, the number of inosine in poly(A) RNA isolated from mouse lung and spleen was significantly increased in correlating with the induction of ADARs' editing activity. The in vitro synthesized RNA which did not contain inosine was edited by thymus extracts and the generation of inosine was greatly increased after editing in LPS treated thymus extract. Take together, these data suggest that A-to-I RNA editing by ADARs may play an important role in pathogenesis of inflammation. The existence of high level of I-mRNA also suggests that more protein isoforms might be generated from a single gene via adenosine deamination by ADARs during inflammatory stress.
机译:A-to-I RNA编辑是最近发现的通过腺苷脱氨对mRNA进行转录后修饰的过程,该过程导致产生基因组中非固有的蛋白质。本研究旨在确定在急性炎症中A-to-I RNA编辑的作用。发现内毒素刺激过程中,小鼠肺,脾,胸腺和淋巴结中RNA酶ADAR的A到I酶活性被上调。重要的是,从小鼠肺和脾中分离出来的poly(A)RNA中的肌苷数量显着增加,这与ADARs编辑活性的诱导有关。胸腺提取物编辑了不含肌苷的体外合成RNA,在LPS处理的胸腺提取物中编辑后,肌苷的生成大大增加。综上所述,这些数据表明,ADAR对A-to-I RNA的编辑可能在炎症的发病机理中起重要作用。高水平的I-mRNA的存在还表明,在炎性应激期间,通过ADAR进行腺苷脱氨,单个基因可能会产生更多的蛋白同工型。

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