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Public Library of Science, PLoS ONE, 1(12), p. e0170097, 2017

DOI: 10.1371/journal.pone.0170097

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Sensitization of TRPA1 by Protein Kinase A

Journal article published in 2017 by Jannis E. Meents, Michael J. M. Fischer ORCID, Peter A. McNaughton
This paper is available in a repository.
This paper is available in a repository.

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Abstract

The TRPA1 ion channel is expressed in nociceptive (pain-sensitive) somatosensory neurons and is activated by a wide variety of chemical irritants, such as acrolein in smoke or isothiocyanates in mustard. Here, we investigate the enhancement of TRPA1 function caused by inflammatory mediators, which is thought to be important in lung conditions such as asthma and COPD. Protein kinase A is an important kinase acting downstream of inflammatory mediators to cause sensitization of TRPA1. By using site-directed mutagenesis, patch-clamp electrophysiology and calcium imaging we identify four amino acid residues, S86, S317, S428, and S972, as the principal targets of PKA-mediated phosphorylation and sensitization of TRPA1.