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酿酒酵母中 20S 蛋白酶体激活因子的缺失下调了对基因组完整性至关重要的基因,增加了 DNA 损伤,并选择性地使细胞对具有不同作用机制的药物敏感。

Loss of a 20S proteasome activator in Saccharomyces cerevisiae downregulates genes important for genomic integrity, increases DNA damage, and selectively sensitizes cells to agents with diverse mechanisms of action.

机构信息

Department of Microbiology and Immunology, City University of New York Sophie Davis School of Biomedical Education, City College, New York, NY 10031-9101, USA.

出版信息

G3 (Bethesda). 2012 Aug;2(8):943-59. doi: 10.1534/g3.112.003376. Epub 2012 Aug 1.

Abstract

Cytoprotective functions of a 20S proteasome activator were investigated. Saccharomyces cerevisiae Blm10 and human 20S proteasome activator 200 (PA200) are homologs. Comparative genome-wide analyses of untreated diploid cells lacking Blm10 and growing at steady state at defined growth rates revealed downregulation of numerous genes required for accurate chromosome structure, assembly and repair, and upregulation of a specific subset of genes encoding protein-folding chaperones. Blm10 loss or truncation of the Ubp3/Blm3 deubiquitinating enzyme caused massive chromosomal damage and cell death in homozygous diploids after phleomycin treatments, indicating that Blm10 and Ubp3/Blm3 function to stabilize the genome and protect against cell death. Diploids lacking Blm10 also were sensitized to doxorubicin, hydroxyurea, 5-fluorouracil, rapamycin, hydrogen peroxide, methyl methanesulfonate, and calcofluor. Fluorescently tagged Blm10 localized in nuclei, with enhanced fluorescence after DNA replication. After DNA damage that caused a classic G2/M arrest, fluorescence remained diffuse, with evidence of nuclear fragmentation in some cells. Protective functions of Blm10 did not require the carboxyl-terminal region that makes close contact with 20S proteasomes, indicating that protection does not require this contact or the truncated Blm10 can interact with the proteasome apart from this region. Without its carboxyl-terminus, Blm10((-339aa)) localized to nuclei in untreated, nonproliferating (G(0)) cells, but not during G(1) S, G(2), and M. The results indicate Blm10 functions in protective mechanisms that include the machinery that assures proper assembly of chromosomes. These essential guardian functions have implications for ubiquitin-independent targeting in anticancer therapy. Targeting Blm10/PA200 together with one or more of the upregulated chaperones or a conventional treatment could be efficacious.

摘要

我们研究了 20S 蛋白酶体激活剂的细胞保护功能。酿酒酵母 Blm10 和人 20S 蛋白酶体激活剂 200(PA200)是同源物。对未经处理的二倍体细胞进行全基因组比较分析,这些细胞在稳定生长状态下以特定的生长速率生长,结果显示,许多与染色体结构、组装和修复准确相关的基因下调,而特定亚组编码蛋白折叠伴侣的基因上调。Blm10 缺失或 Ubp3/Blm3 去泛素化酶截断导致同源二倍体在博来霉素处理后大量染色体损伤和细胞死亡,表明 Blm10 和 Ubp3/Blm3 功能是稳定基因组并防止细胞死亡。缺乏 Blm10 的二倍体也对阿霉素、羟基脲、5-氟尿嘧啶、雷帕霉素、过氧化氢、甲磺酸甲酯和 Calcofluor 敏感。荧光标记的 Blm10 定位于细胞核中,在 DNA 复制后荧光增强。在引起经典 G2/M 期阻滞的 DNA 损伤后,荧光仍然弥散,一些细胞中出现核碎裂的证据。Blm10 的保护功能不需要与 20S 蛋白酶体紧密接触的羧基末端区域,这表明保护不需要这种接触,或者截断的 Blm10 可以在没有这个区域的情况下与蛋白酶体相互作用。没有其羧基末端,Blm10((-339aa))在未经处理的非增殖(G(0))细胞中定位于细胞核,但在 G(1)S、G(2)和 M 期则不定位。结果表明,Blm10 在保护机制中发挥作用,包括确保染色体正确组装的机制。这些必要的保护功能对非泛素依赖性靶向抗癌治疗具有重要意义。靶向 Blm10/PA200 与一个或多个上调的伴侣蛋白或常规治疗联合使用可能是有效的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/beca/3411250/2442c2ffe21d/943f1.jpg

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