How anchoring proteins shape pain

Michael J. M. Fischer*, Peter A. McNaughton

*Corresponding author for this work

Research output: Contribution to journalLiterature reviewpeer-review

6 Citations (Scopus)

Abstract

Cellular responsiveness to external stimuli can be altered by extracellular mediators which activate membrane receptors, in turn signalling to the intracellular space via calcium, cyclic nucleotides, membrane lipids or enzyme activity. These signalling events trigger a cascade leading to an effector which can be a channel, an enzyme or a transcription factor. The effectiveness of these intracellular events is enhanced when they are maintained in close proximity by anchoring proteins, which assemble complexes of signalling molecules such as kinases together with their targets, and in this way enhance both the speed and the precision of intracellular signalling. The A kinase anchoring protein (AKAP) family are adaptor proteins originally named for their ability to associate Protein Kinase A and its targets, but several other enzymes bound by AKAPs have now been found and a wide variety of target structures has been described. This review provides an overview of anchoring proteins involved in pain signalling. The key anchoring proteins and their ion channel targets in primary sensory neurons responding to painful stimuli (nociceptors) are discussed.

Original languageEnglish
Pages (from-to)316-322
Number of pages7
JournalPharmacology and Therapeutics
Volume143
Issue number3
DOIs
Publication statusPublished - Sept 2014

Keywords

  • Accessory protein
  • AKAP
  • Pain
  • Scaffolding protein
  • Sensitisation
  • DORSAL-ROOT GANGLION
  • SENSING ION-CHANNEL
  • KINASE-A
  • NEUROPATHIC PAIN
  • SYNAPTIC PLASTICITY
  • INFLAMMATORY HYPERALGESIA
  • MICE LACKING
  • K+ CHANNELS
  • CYCLIC-AMP
  • THERMAL HYPERALGESIA

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