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氧化应激诱导在酿酒酵母中Na+毒性中的作用及其与Ca2+依赖性但无需钙调磷酸酶功能部分抑制的机制的关系。

Involvement of oxidative stress induction in Na+ toxicity and its relation to the inhibition of a Ca2+ -dependent but calcineurin-independent mechanism in Saccharomyces cerevisiae.

作者信息

Tanaka Toshio, Nishio Kyoichi, Usuki Yoshinosuke, Fujita Ken-Ichi

机构信息

Department of Biology and Geosciences, Graduate School of Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka 558-8585, Japan.

出版信息

J Biosci Bioeng. 2006 Jan;101(1):77-9. doi: 10.1263/jbb.101.77.

Abstract

Uridine 5'-hexadecylphosphate (UMPC16) inhibited the growth of Saccharomyces cerevisiae under a hypersaline stress condition with Na+ more strongly than the calcineurin inhibitor cyclosporine A (CsA). Additional Ca2+ supplementation similarly suppressed the inhibitory activities of UMPC16 and CsA on yeast cell growth in a medium with Na+. UMPC16, but not CsA, accelerated mitochondrial reactive oxygen species (ROS) generation in combination with Na+, suggesting its inhibition of a Ca2+ -dependent but calcineurin-independent mechanism for protection against Na+ toxicity.

摘要

5'-十六烷基磷酸尿苷(UMPC16)在高盐胁迫条件下(Na+存在时)对酿酒酵母生长的抑制作用比钙调神经磷酸酶抑制剂环孢素A(CsA)更强。额外补充Ca2+同样能抑制UMPC16和CsA对含Na+培养基中酵母细胞生长的抑制活性。UMPC16而非CsA,在与Na+共同作用时会加速线粒体活性氧(ROS)的生成,这表明其抑制了一种依赖Ca2+但不依赖钙调神经磷酸酶的机制来抵御Na+毒性。

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