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在异烟肼诱导的HL-60细胞对过氧化氢刺激的细胞保护过程中获取的全球蛋白质表达数据集。

Global protein expression dataset acquired during isoniazid-induced cytoprotection against H2O2 challenge in HL-60 cells.

作者信息

Khan Saifur R, Baghdasarian Argishti, Fahlman Richard P, Siraki Arno G

机构信息

Faculty of Pharmacy and Pharmaceutical Sciences, University of Alberta, Edmonton, Canada.

Department of Biochemistry, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, Canada; Department of Oncology, Faculty of Medicine & Dentistry, University of Alberta, Edmonton, Canada.

出版信息

Data Brief. 2016 Jan 29;6:823-8. doi: 10.1016/j.dib.2016.01.035. eCollection 2016 Mar.

DOI:10.1016/j.dib.2016.01.035
PMID:26937455
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4749934/
Abstract

Isoniazid (INH) is one of the first-line anti-tuberculosis drugs. Its effect on oxidative stress, however, is unknown. Here we used a model of oxidative stress by employing glucose/glucose oxidase (GOx), which (based on the availability of glucose and oxygen) is known to produce H2O2. This reaction induces oxidative stress culminating in necrotic cell death in HL-60 cells (a human promyelocytic leukemia cell line). The changes in protein levels have been quantified using global proteome expression changes through stable isotope labeling by amino acids in cell culture (SILAC) followed by LC-MS/MS analysis. A total of 1459 and 1712 proteins were identified in forward and reverse experiments, respectively. However, only 390 proteins were reproducibly identified in both samples. These 390 proteins were taken into account for further analysis which has been described in "Cytoprotective effect of isoniazid against H2O2 derived injury in HL-60 cells" [1].

摘要

异烟肼(INH)是一线抗结核药物之一。然而,其对氧化应激的影响尚不清楚。在此,我们通过使用葡萄糖/葡萄糖氧化酶(GOx)建立了一种氧化应激模型,已知该模型(基于葡萄糖和氧气的可用性)会产生过氧化氢。该反应诱导氧化应激,最终导致HL-60细胞(一种人早幼粒细胞白血病细胞系)发生坏死性细胞死亡。通过细胞培养中氨基酸的稳定同位素标记(SILAC)随后进行LC-MS/MS分析,利用全球蛋白质组表达变化对蛋白质水平的变化进行了定量。在正向和反向实验中分别鉴定出1459和1712种蛋白质。然而,两个样品中可重复鉴定出的蛋白质只有390种。在“异烟肼对HL-60细胞中过氧化氢所致损伤的细胞保护作用”[1]中描述了对这390种蛋白质进行进一步分析的情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bc/4749934/7302e038bc05/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bc/4749934/526a60d37109/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bc/4749934/7302e038bc05/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bc/4749934/526a60d37109/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d1bc/4749934/7302e038bc05/gr2.jpg

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引用本文的文献

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本文引用的文献

1
Cytoprotective effect of isoniazid against H2O2 derived injury in HL-60 cells.异烟肼对HL-60细胞中过氧化氢所致损伤的细胞保护作用。
Chem Biol Interact. 2016 Jan 25;244:37-48. doi: 10.1016/j.cbi.2015.11.026. Epub 2015 Nov 30.
2
Proteomic profile of aminoglutethimide-induced apoptosis in HL-60 cells: Role of myeloperoxidase and arylamine free radicals.氨鲁米特诱导HL-60细胞凋亡的蛋白质组学特征:髓过氧化物酶和芳胺自由基的作用
Chem Biol Interact. 2015 Sep 5;239:129-38. doi: 10.1016/j.cbi.2015.06.020. Epub 2015 Jun 20.
3
Current status and future prospects of toxicogenomics in drug discovery.
毒理基因组学在药物发现中的现状与未来前景
Drug Discov Today. 2014 May;19(5):562-78. doi: 10.1016/j.drudis.2013.11.001. Epub 2013 Nov 8.