Sensitization of TRPA1 by Protein Kinase A

被引：42

作者：

Meents, Jannis E. ^{[1
,2
]}

Fischer, Michael J. M. ^{[1
,3
,4
]}

McNaughton, Peter A. ^{[1
,5
]}

机构：

[1] Univ Cambridge, Dept Pharmacol, Cambridge, England

[2] Uniklin RWTH Aachen, Inst Physiol, Aachen, Germany

[3] Univ Erlangen Nurnberg, Inst Physiol & Pathophysiol, Erlangen, Germany

[4] Med Univ Wien, Ctr Physiol & Pharmacol, Vienna, Austria

[5] Kings Coll London, Wolfson Ctr Age Related Dis, London, England

来源：

PLOS ONE | 2017年 / 12卷 / 01期

基金：

英国生物技术与生命科学研究理事会;

关键词：

ION-CHANNEL TRPA1; INFLAMMATORY HYPERALGESIA; SENSORY NEURONS; CALCIUM-IONS; RECEPTOR; ACTIVATION; PHOSPHORYLATION; TRPV1; PAIN; SITE;

D O I：

10.1371/journal.pone.0170097

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页数：15

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