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磷酸烯醇式丙酮酸羧激酶参与家蚕核型多角体病毒的抗病毒免疫。

Phosphoenolpyruvate carboxykinase is involved in antiviral immunity against Bombyx mori nucleopolyhedrovirus.

作者信息

Guo Huizhen, Xu Guowen, Wang Bingbing, Xia Fei, Sun Qiang, Wang Yumei, Xie Enyu, Lu Zhongyan, Jiang Liang, Xia Qingyou

机构信息

State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China; Chongqing Key Laboratory of Sericultural Science, Chongqing Engineering and Technology Research Center for Novel Silk Materials, Southwest University, Chongqing, 400715, China.

State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing, 400715, China.

出版信息

Dev Comp Immunol. 2019 Mar;92:193-198. doi: 10.1016/j.dci.2018.11.015. Epub 2018 Nov 22.

Abstract

Phosphoenolpyruvate carboxykinase (PEPCK) has cytoplasmic isoform (PEPCK-C) and a mitochondrial isoform (PEPCK-M). PEPCK-C plays an important role in gluconeogenesis, but the function of PEPCK-M is largely unknown. In this study, we cloned two isoforms of PEPCK (BmPEPCK-1 and BmPEPCK-2; both of PEPCK-M) from the lepidopteran model Bombyx mori. BmPEPCK-1 and BmPEPCK-2 were adjacently located in the silkworm genome, and both contained 13 exons. The main difference in the sequences was the 13th exon and 3'UTR. The expression of BmPEPCK-1 was higher than that of BmPEPCK-2, the overexpression of which did not affect BmNPV proliferation. The expression levels of BmPEPCK-2 and ATG6/7/8/13 decreased after BmNPV infection. Overexpression of BmPEPCK-2 increased the expression of ATG6/7/8 and significantly decreased viral fluorescence and content, suggesting that BmPEPCK-2 suppressed the multiplication of BmNPV by increasing ATGs expression. These results revealed that PEPCK-M has an important function in antiviral immunity.

摘要

磷酸烯醇式丙酮酸羧激酶(PEPCK)有细胞质异构体(PEPCK-C)和线粒体异构体(PEPCK-M)。PEPCK-C在糖异生中起重要作用,但PEPCK-M的功能在很大程度上尚不清楚。在本研究中,我们从鳞翅目模式生物家蚕中克隆了PEPCK的两种异构体(BmPEPCK-1和BmPEPCK-2;均为PEPCK-M)。BmPEPCK-1和BmPEPCK-2在蚕基因组中相邻定位,且都包含13个外显子。序列的主要差异在于第13个外显子和3'非翻译区。BmPEPCK-1的表达高于BmPEPCK-2,其过表达不影响家蚕核型多角体病毒(BmNPV)增殖。BmNPV感染后,BmPEPCK-2和自噬相关基因6/7/8/13的表达水平下降。BmPEPCK-2的过表达增加了自噬相关基因6/7/8的表达,并显著降低了病毒荧光和病毒含量,表明BmPEPCK-2通过增加自噬相关基因的表达来抑制BmNPV的增殖。这些结果揭示了PEPCK-M在抗病毒免疫中具有重要功能。

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