热休克转录因子HSF-1保护秀丽隐杆线虫免受过氧化应激

Q2 Medicine
Francesco A. Servello, Javier Apfeld
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引用次数: 0

摘要

细胞诱导保守的防御机制保护它们免受氧化应激。这些防御在多细胞生物中是如何被调节的还不完全清楚。在这里,我们发现热休克转录因子HSF-1保护秀丽隐杆线虫免受环境过氧化引起的氧化应激。在应对热休克或温和的温度升高时,HSF-1保护线虫免受随后的过氧化应激,其方式取决于HSF-1的活化结构域。在恒定温度下,HSF-1保护线虫免受过氧化胁迫,不依赖于其转激活结构域,可能是通过诱导asp-4/cathepsin和dapk-1/dapk的表达。因此,两种不同的hsf -1依赖过程保护秀丽隐杆线虫免受过氧化应激。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The heat shock transcription factor HSF-1 protects Caenorhabditis elegans from peroxide stress

Cells induce conserved defense mechanisms that protect them from oxidative stress. How these defenses are regulated in multicellular organisms is incompletely understood. Here, we show that the heat shock transcription factor HSF-1 protects the nematode Caenorhabditis elegans from the oxidative stress caused by environmental peroxide. In response to a heat shock or a mild temperature increase, HSF-1 protects the nematodes from subsequent peroxide stress in a manner that depends on HSF-1’s transactivation domain. At constant temperature, HSF-1 protects the nematodes from peroxide stress independently of its transactivation domain, likely by inducing the expression of asp-4/cathepsin and dapk-1/dapk. Thus, two distinct HSF-1-dependent processes protect C. elegans from peroxide stress.

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来源期刊
Translational Medicine of Aging
Translational Medicine of Aging Medicine-Geriatrics and Gerontology
CiteScore
5.30
自引率
0.00%
发文量
2
审稿时长
103 days
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