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Modulation of TRPA1 channel activity by Cdk5 in sensory neurons

Michael A Sulak1, Monica Ghosh2, Pritam Sinharoy3

  • 1a Department of Human Genetics , University of Chicago , Chicago , IL , USA.

Channels (Austin, Tex.)
|January 9, 2018
PubMed

Insights

Cyclin-dependent kinase 5 (Cdk5) modulates the activity of the TRPA1 channel, a key player in pain signaling. Cdk5 inhibition reduces TRPA1 responses, suggesting a role in pain modulation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Transient receptor potential cation channel, subfamily A, member 1 (TRPA1) is activated by noxious stimuli.
  • Cyclin-dependent kinase 5 (Cdk5) is implicated in pain signaling pathways.

Purpose of the Study:

  • To investigate the role of Cdk5 in modulating TRPA1 channel activity.

Main Methods:

  • Experiments were conducted using mouse dorsal root ganglion (DRG) sensory neurons and transfected HEK293 cells.
  • Cdk5 activity was inhibited and TRPA1 phosphorylation was assessed.
  • In vitro kinase assays were performed using immunopurified Cdk5 and TRPA1 peptide substrates.

Main Results:

  • Cdk5 inhibition attenuated TRPA1 responses to agonists in mouse DRG neurons.
  • Active Cdk5 correlated with increased TRPA1 phosphorylation in HEK293 cells, sensitive to roscovitine.
  • Phosphorylation was absent in a mouse mutant TRPA1 (S449A) and Cdk5 phosphorylated a human TRPA1 peptide at S448A in vitro.

Conclusions:

  • Cdk5 plays a role in modulating TRPA1 channel activity.
  • Cdk5-mediated phosphorylation of TRPA1 may be a mechanism influencing pain signaling.
Keywords:
Ca2+ signalingCdk5DRG neuronsTRPA1ion channel

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