Journal
PLOS ONE
Volume 12, Issue 1, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0170097
Keywords
-
Categories
Funding
- Biotechnology and Biological Sciences Research Council, UK (BBSRC)
- Department of Pharmacology Cambridge
- Ernst Schering Foundation
- Deutsche Schmerzgesellschaft e.V.
- German Academic Exchange Service
- Alexander von Humboldt Foundation
- BBSRC [BB/L002787/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/L002787/1] Funding Source: researchfish
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available