MassIVE MSV000085562

Partial Public

Regulators of TNF alpha Mediated Insulin Resistance Elucidated by Quantitative Proteomics

Description

Obesity is a growing epidemic worldwide and is a major risk factor for several chronic diseases, including diabetes, kidney disease, heart disease, and cancer. The global epidemic of obesity has been accompanied with a dramatic increase in the incidence and prevalence of type 2 diabetes mellitus (T2DM). Obesity often leads to T2D, via the increased production of proinflammatory cytokines such as tumor necrosis factor alpha. Our study combines different proteomic techniques to investigate the changes in the global proteome, secretome and phosphoproteome of adipocytes under chronic inflammation condition, as well as fundamental cross-talks between different cellular pathways regulated by chronic TNF alpha exposure. Our results show that many key regulator proteins of the canonical and non-canonical NF-kB pathways, such as Nfkb2, and its downstream effectors, including Csf-1 and Lgals3bp, directly involved in leukocyte migration and invasion, were significantly upregulated at the intra and extracellular levels, culminating in the progression of inflammation. Our data provides evidence of several key proteins that play a role in the development of insulin resistance. [doi:10.25345/C54Q5W] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: Proteomics ; phosphoproteomics ; secretomics ; tumor necrosis factor ; insulin resistance ; 3T3-L1 cell

Contact

Principal Investigators:
(in alphabetical order)
Uma K Aryal, Purdue University, United States
Submitting User: uma_aryal
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Distinct protein accessions are counted across all files submitted in the "Statistical Analysis of Quantified Analytes" category having a "Protein" column in this dataset.

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