Tumor necrosis factor-α- and interleukin-1-induced cellular responses: Coupling proteomic and genomic information

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

Research output: Contribution to journalArticle

8 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)2176-2185
Number of pages10
JournalJournal of Proteome Research
Issue number6
StatePublished - Jun 2007



  • Cell cycle arrest
  • Interleukin-1
  • Mass spectrometry
  • Microarray
  • Permeability transition pore
  • Protein interaction network
  • Tumor necrosis factor-alpha

ASJC Scopus subject areas

  • Genetics
  • Biotechnology
  • Biochemistry

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