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鉴定一种来自橙点石斑鱼(Epinephelus coioides)的 Bcl-xL 同源物,该同源物参与 SGIV 诱导的非凋亡性细胞死亡。

Identification of a Bcl-xL homolog from orange-spotted grouper (Epinephelus coioides) involved in SGIV-induced nonapoptotic cell death.

机构信息

College of Fishery, Guangdong Ocean University, Zhanjiang, 524088, China; Guangdong Provincial Key Laboratory of Pathogenic Biology and Epidemiology for Aquatic Economic Animals, Zhanjiang, 524088, China; Guangdong Key Laboratory of Control for Diseases of Aquatic Economic Animals, Zhanjiang, 524088, China.

Zhaoqing Dahuanong Biology Medicine Co., Ltd., China.

出版信息

Fish Shellfish Immunol. 2018 Dec;83:436-442. doi: 10.1016/j.fsi.2018.09.053. Epub 2018 Sep 21.

Abstract

Bcl-2 family proteins play essential roles in modulating immune response and controlling cells' fate. Bcl-xL is one of anti-apoptotic protein in this family. In this study, a new Bcl-xL homolog (EcBcl-xL) was identified and characterized from orange-spotted grouper, Epinephelus coioides. EcBcl-xL encoded a 221 amino acid peptides that shared 86% identity to Larimichthys crocea Bcl-xL protein, contained four conserved BH domains and one transmembrane region. The predicted three-dimensional structure of EcBcl-xL was similar with Homo sapiens Bcl-xL. EcBcl-xL widely expressed in all tested tissues with highest expression in head kidney. Its expression level was significantly up-regulated after SGIV infection in vivo. Furthermore, overexpression of EcBcl-xL could inhibit SGIV-induced nonapoptotic cell death and suppressed viral genes transcriptions in GS cells. Our findings suggested that EcBcl-xL might play a role during virus infection through modulating SGIV-induced nonapoptotic cell death.

摘要

Bcl-2 家族蛋白在调节免疫反应和控制细胞命运方面发挥着重要作用。Bcl-xL 是该家族中的一种抗凋亡蛋白。本研究从青石斑鱼中鉴定并表征了一种新的 Bcl-xL 同源物(EcBcl-xL)。EcBcl-xL 编码一个 221 个氨基酸的肽段,与 Larimichthys crocea Bcl-xL 蛋白的同源性为 86%,含有四个保守的 BH 结构域和一个跨膜区。EcBcl-xL 的预测三维结构与人类 Bcl-xL 相似。EcBcl-xL 在所有检测的组织中广泛表达,在头肾中表达量最高。在体内 SGIV 感染后,其表达水平显著上调。此外,EcBcl-xL 的过表达可抑制 SGIV 诱导的非凋亡性细胞死亡,并抑制 GS 细胞中病毒基因的转录。我们的研究结果表明,EcBcl-xL 可能通过调节 SGIV 诱导的非凋亡性细胞死亡在病毒感染过程中发挥作用。

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