Tumor Necrosis Factor-alpha- and Interleukin-1-induced Cellular Responses: Coupling Proteomic and Genomic Information

Overview

Journal J Proteome Res

Publisher American Chemical Society

Specialty Biochemistry

Date 2007 May 17

PMID 17503796

Citations 38

Authors

Lee W Ott

Katheryn A Resing

Alecia W Sizemore

Joshua W Heyen

Ross R Cocklin

Nathan M Pedrick

H Cary Woods

Jake Y Chen

Mark G Goebl

Frank A Witzmann

Maureen A Harrington

Affiliations

Soon will be listed here.

Abstract

The pro-inflammatory cytokines, Tumor Necrosis Factor-alpha (TNFalpha) 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. TNFalpha- and IL-1-induced changes in gene expression are mediated by similar transcription factors; however, TNFalpha 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 TNFalpha and IL-1 regulate different processes. A large-scale proteomic analysis of TNFalpha- and IL-1-induced responses was undertaken to identify processes uniquely regulated by TNFalpha and IL-1. When combined with genomic studies, our results indicate that TNFalpha, but not IL-1, mediates cell cycle arrest.

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