A high-throughput quantitative multiplex kinase assay for monitoring information flow in signaling networks: application to sepsis-apoptosis

Mol Cell Proteomics. 2003 Jul;2(7):463-73. doi: 10.1074/mcp.M300045-MCP200. Epub 2003 Jun 26.

Abstract

To treat complex human diseases effectively, a systems-level approach is needed to understand the interplay of environmental cues, intracellular signals, and cellular behaviors that underlie disease states. This approach requires high-throughput, multiplex techniques that measure quantitative temporal variations of multiple protein activities in the intracellular signaling network. Here, we describe a single microtiter-based format that simultaneously quantifies protein kinase activities in the phosphatidylinositol 3-kinase pathway (Akt), nuclear factor-kappaB pathway (IKK), and three core mitogen-activated protein kinase pathways (ERK, JNK1, MK2). These parallel high-throughput assays are stringently linear, redundantly specific, reproducible, and sensitive compared with classical low-throughput techniques. When applied to a model of sepsis-induced colon epithelial apoptosis, this approach identified a late phase of Akt activity as a critical mediator of cell survival that quantitatively contributed to the efficacy of insulin as an anti-apoptotic cue. Thus, sampling parallel nodes in the intracellular signaling network identified part of the molecular mechanism underlying the efficacy of insulin in the treatment of human sepsis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Biological Assay
  • Cell Survival / drug effects
  • HT29 Cells
  • HeLa Cells
  • Humans
  • I-kappa B Kinase / metabolism*
  • Insulin / pharmacology
  • Insulin / therapeutic use
  • Intracellular Signaling Peptides and Proteins
  • Mitogen-Activated Protein Kinase 8 / metabolism*
  • Protein Kinases / metabolism*
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Reproducibility of Results
  • Sensitivity and Specificity
  • Sepsis / drug therapy
  • Sepsis / physiopathology
  • Signal Transduction*
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Insulin
  • Intracellular Signaling Peptides and Proteins
  • Tumor Necrosis Factor-alpha
  • Protein Kinases
  • MAP-kinase-activated kinase 2
  • Protein Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • I-kappa B Kinase
  • Mitogen-Activated Protein Kinase 8