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胰岛素/胰岛素样生长因子-1信号通路的减弱以及……的缺失促进了……中重复DNA的沉默。 (注:原文部分内容缺失,翻译可能不太完整准确)

Reduced insulin/IGF-1 signaling and loss of promote repetitive DNA silencing in .

作者信息

Ewe Chee Kiang, Teichman Guy, Rechavi Oded

机构信息

School of Neurobiology, Biochemistry and Biophysics, Wise Faculty of Life Sciences & Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Tel Aviv, Israel.

出版信息

MicroPubl Biol. 2025 Aug 6;2025. doi: 10.17912/micropub.biology.001747. eCollection 2025.

Abstract

Non-coding small RNAs and Argonaute proteins mediate conserved defenses against foreign genetic elements. mutants in the insulin/IGF-1 signaling (IIS) have previously been shown to exhibit an enhanced response to exogenous RNAi. Here, we found that the loss of IIS via enhances transgene silencing, which is reversed by knocking out . Similarly, mutants show enhanced RNAi and upregulation of antiviral RNAi pathway. and mutations exhibit additive effects, and loss of restores transgene expression in mutants but not in mutants, suggesting that these genes act in parallel. RNAi gene expression in mutants lacked a consistent pattern, suggesting IIS may regulate RNAi components via post-translational mechanisms.

摘要

非编码小RNA和AGO蛋白介导对外来遗传元件的保守防御。先前已表明胰岛素/IGF-1信号通路(IIS)中的突变体对外源RNA干扰表现出增强的反应。在这里,我们发现通过……导致IIS缺失会增强转基因沉默,而敲除……可逆转这种情况。同样,……突变体表现出增强的RNA干扰和抗病毒RNA干扰途径的上调。……和……突变表现出累加效应,并且……缺失可恢复……突变体中的转基因表达,但不能恢复……突变体中的转基因表达,这表明这些基因平行发挥作用。……突变体中的RNA干扰基因表达缺乏一致模式,表明IIS可能通过翻译后机制调节RNA干扰组分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8733/12368607/f696b45c3ec5/25789430-2025-micropub.biology.001747.jpg

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