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基于稳定同位素标记氨基酸细胞培养技术的MKK3基因敲除小鼠胚胎成纤维细胞的蛋白质谱数据。

SILAC based protein profiling data of MKK3 knockout mouse embryonic fibroblasts.

作者信息

Srivastava Anup, Shinn Amanda S, Lam TuKiet T, Lee Patty J, Mannam Praveen

机构信息

Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8057, USA.

MS & Proteomics Resource at Yale University, WM Keck Foundation Biotechnology Resource Laboratory, Department of Molecular Biophysics and Biochemistry, New Haven, CT 06520-8057, USA.

出版信息

Data Brief. 2016 Mar 2;7:418-22. doi: 10.1016/j.dib.2016.02.034. eCollection 2016 Jun.

DOI:10.1016/j.dib.2016.02.034
PMID:26977448
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4782019/
Abstract

This data article reports changes in the phospho and total proteome of MKK3 knock out (MKK3(-) (/) (-)) mouse embryonic fibroblasts (MEFs). The dataset generated highlights the changes at protein level which can be helpful for understanding targets of the MAP kinase signaling pathway. Data was collected after TiO2-based phosphopeptide enrichment of whole cell lysate at baseline condition with bottom-up SILAC-based LC MS/MS quantitative mass spectrometry. We report all the proteins and peptides identified and quantified in MKK3(-/-) and WT MEFs. The altered pathways in MKK3(-/-) MEFs were analyzed by Database for Annotation, Visualization and Integrated Discovery (DAVID, v6.7) and Ingenuity Pathway Analysis (IPA) and are presented as a table and graph, respectively. The data reported here is related to the published work [1]. All the associated mass spectrometry data has been deposited in the Yale Protein Expression Database (YPED) with the web-link to the data: http://yped.med.yale.edu/repository/ViewSeriesMenu.do;jsessionid=6A5CB07543D8B529FAE8C3FCFE29471D?series_id=5044&series_name=MMK3+Deletion+in+MEFs.

摘要

本数据文章报告了MKK3基因敲除(MKK3(-)/(-))小鼠胚胎成纤维细胞(MEF)的磷酸化蛋白质组和总蛋白质组的变化。所生成的数据集突出了蛋白质水平的变化,这有助于理解丝裂原活化蛋白激酶信号通路的靶点。在基线条件下,通过基于二氧化钛的磷酸肽富集全细胞裂解物,并采用自下而上的基于稳定同位素标记氨基酸的细胞培养(SILAC)液相色谱-质谱联用(LC MS/MS)定量质谱法收集数据。我们报告了在MKK3(-/-)和野生型(WT)MEF中鉴定和定量的所有蛋白质和肽段。通过注释、可视化和综合发现数据库(DAVID,v6.7)和 Ingenuity 通路分析(IPA)分别对MKK3(-/-) MEF中改变的通路进行了分析,并以表格和图表形式呈现。此处报告的数据与已发表的工作[1]相关。所有相关的质谱数据已存入耶鲁蛋白质表达数据库(YPED),数据的网络链接为:http://yped.med.yale.edu/repository/ViewSeriesMenu.do;jsessionid=6A5CB07543D8B529FAE8C3FCFE29471D?series_id=5044&series_name=MMK3+Deletion+in+MEFs 。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc5e/4782019/70f390523a7c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc5e/4782019/5446ddaadf1e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc5e/4782019/70f390523a7c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc5e/4782019/5446ddaadf1e/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc5e/4782019/70f390523a7c/gr2.jpg

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引用本文的文献

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Proteomics data on MAP Kinase Kinase 3 knock out bone marrow derived macrophages exposed to cigarette smoke extract.关于暴露于香烟烟雾提取物的丝裂原活化蛋白激酶激酶3基因敲除骨髓来源巨噬细胞的蛋白质组学数据。
Data Brief. 2017 Jun 7;13:320-325. doi: 10.1016/j.dib.2017.05.049. eCollection 2017 Aug.

本文引用的文献

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2
MKK3 mediates inflammatory response through modulation of mitochondrial function.MKK3通过调节线粒体功能介导炎症反应。
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Endothelial MKK3 is a critical mediator of lethal murine endotoxemia and acute lung injury.内皮细胞 MKK3 是致命性的小鼠内毒素血症和急性肺损伤的关键介质。
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MKK3/6-p38 MAPK signaling is required for IL-1beta and TNF-alpha-induced RANKL expression in bone marrow stromal cells.MKK3/6-p38丝裂原活化蛋白激酶信号通路是白细胞介素-1β和肿瘤坏死因子-α诱导骨髓基质细胞中核因子κB受体活化因子配体表达所必需的。
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