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氧化延伸因子 G 敏感性的改变可保护集胞藻 PCC 6803 的光系统 II 免受光抑制。

A change in the sensitivity of elongation factor G to oxidation protects photosystem II from photoinhibition in Synechocystis sp. PCC 6803.

机构信息

Department of Biochemistry and Molecular Biology, Graduate School of Science and Engineering, Saitama University, Sakura-ku, Saitama, Japan.

出版信息

FEBS Lett. 2012 Mar 23;586(6):778-83. doi: 10.1016/j.febslet.2012.01.042. Epub 2012 Jan 28.

Abstract

The repair of photosystem II (PSII) after photodamage is particularly sensitive to oxidative stress and inhibition of such repair is associated with the oxidation of specific cysteine residues in elongation factor G (EF-G), a key translation factor, in the cyanobacterium Synechocystis sp. PCC 6803. Expression of mutated EF-G with a target cysteine residue replaced by serine in Synechocystis resulted in the protection of PSII from photoinhibition. This protection was attributable to the enhanced repair of PSII via acceleration of the synthesis of the D1 protein, which might have been due to reduced sensitivity of protein synthesis to oxidative stress.

摘要

类囊体 II(PSII)的光损伤修复对氧化应激特别敏感,并且在蓝藻集胞藻 PCC 6803 中,这种修复受到伸长因子 G(EF-G)中特定半胱氨酸残基氧化的抑制,EF-G 是一种关键的翻译因子。在集胞藻中表达具有目标半胱氨酸残基被丝氨酸取代的突变 EF-G,可防止 PSII 光抑制。这种保护归因于通过加速 D1 蛋白的合成来增强 PSII 的修复,这可能是由于蛋白质合成对氧化应激的敏感性降低所致。

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