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Data Brief. 2017 Jun 7;13:320-325. doi: 10.1016/j.dib.2017.05.049. eCollection 2017 Aug.

Proteomics data on MAP Kinase Kinase 3 knock out bone marrow derived macrophages exposed to cigarette smoke extract.

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Department of Internal Medicine, Yale University School of Medicine, USA.
MS & Proteomics Resource at Yale University, WM Keck Foundation Biotechnology Resource Laboratory, Department of Molecular Biophysics and Biochemistry, New Haven, CT, USA.
Department of Epidemiology & Biostatistics, School of Public Health, Georgia State University, Atlanta, GA, USA.
Division of Translational and Regenerative Medicine, Internal Medicine, University of Arizona, Tucson, AZ, USA.


This data article reports changes in the phosphoproteome and total proteome of cigarette smoke extract (CSE) exposed WT and MAP Kinase Kinase 3 knock out (MKK3-/-) bone marrow derived macrophages (BMDM). The dataset generated is helpful for understanding the mechanism of CSE induced inflammation and the role of MAP kinase signaling pathway. The cellular proteins were labeled with isobaric tags for relative and absolute quantitation (iTRAQ®) reagents and analyzed by LC-MS/MS. The standard workflow module for iTRAQ® quantification within the Proteome Discoverer was utilized for the data analysis. Ingenuity Pathway Analysis (IPA) software and Reactome was used to identify enriched canonical pathways and molecular networks (Mannam et al., 2016) [1]. All the associated mass spectrometry data has been deposited in the Yale Protein Expression Database (YPED) with the web-link to the data:;jsessionid=6A5CB07543D8B529FAE8C3FCFE29471D?series_id=5044&series_name=MMK3+Deletion+in+MEFs.


Cigarette smoke; Inflammation; MKK3; Proteomics; iTRAQ®

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