Dissection of signaling in inflammation: three novel inflammatory regulators

Cold Spring Harb Symp Quant Biol. 2013:78:141-7. doi: 10.1101/sqb.2013.78.020107.

Abstract

Uncontrolled inflammation is a feature of autoimmune diseases and autoinflammatory syndromes and may promote tumorigenesis. Thus, identifying molecules that regulate the signaling pathways triggering, mediating, and suppressing inflammation could be helpful in developing new therapeutic approaches for these debilitating diseases. In this review, we present new information on three molecules with important roles in controlling inflammation: MALT1, Ariadne-2, and acetylcholine. We summarize our current state of knowledge of how these molecules function, and how they are involved in pathways of NF-κB activation or vagal nerve stimulation associated with inflammation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acetylcholine / metabolism
  • Animals
  • Anti-Inflammatory Agents / chemistry
  • Autoimmune Diseases / metabolism
  • Caspases / metabolism
  • Computer Simulation
  • Gene Expression Regulation*
  • Humans
  • Inflammation*
  • Mice
  • Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein
  • NF-kappa B / metabolism
  • Neoplasm Proteins / metabolism
  • Phosphorylation
  • Signal Transduction*
  • Ubiquitin-Protein Ligases / metabolism

Substances

  • Anti-Inflammatory Agents
  • NF-kappa B
  • Neoplasm Proteins
  • ARIH2 protein, human
  • Ubiquitin-Protein Ligases
  • Caspases
  • MALT1 protein, human
  • Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein
  • Acetylcholine