Tumor Necrosis Factor-α- and Interleukin-1-Induced Cellular Responses: Coupling Proteomic and Genomic Information
Authors:
- Lee W. OttLOLee W. Ott
- Katheryn A. ResingKRKatheryn A. Resing
- Alecia W. SizemoreASAlecia W. Sizemore
- Joshua W. HeyenJHJoshua W. Heyen
- Ross R. CocklinRCRoss R. Cocklin
- Nathan M. PedrickNPNathan M. Pedrick
- H. Cary WoodsHWH. Cary Woods
- Jake Y. ChenJCJake Y. Chen
- Mark G. GoeblMGMark G. Goebl
- Frank A. WitzmannFWFrank A. Witzmann
- Maureen A. HarringtonMHMaureen A. Harrington
- 16 May 2007
- journal article
- research article
- Published by American Chemical Society (ACS) in Journal of Proteome Research
- Vol. 6 (6) , 2176-2185
Abstract
The pro-inflammatory cytokines, Tumor Necrosis Factor-alpha (TNFα) and Interleukin-1 (IL-1) mediate the innate immune response. Dysregulation of the innate immune response contributes to the pathogenesis of cancer, arthritis, and congestive heart failure. TNFα- and IL-1-induced changes in gene expression are mediated by similar transcription factors; however, TNFα and IL-1 receptor knock-out mice differ in their sensitivities to a known initiator (lipopolysaccharide, LPS) of the innate immune response. The contrasting responses to LPS indicate that TNFα and IL-1 regulate different processes. A large-scale proteomic analysis of TNFα- and IL-1-induced responses was undertaken to identify processes uniquely regulated by TNFα and IL-1. When combined with genomic studies, our results indicate that TNFα, but not IL-1, mediates cell cycle arrest. Keywords: Tumor Necrosis Factor-alpha • Interleukin-1 • Cell Cycle Arrest • Permeability Transition Pore • Protein Interaction Network • Mass Spectrometry • MicroarrayKeywords
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