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2016 Fiscal Year Final Research Report

pain modulation by AMP kinase through TRP channels and its molecular mechanism

Research Project

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Project/Area Number 26460713
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Pain science
Research InstitutionHyogo University of Health Sciences

Principal Investigator

DAI YI  兵庫医療大学, 薬学部, 教授 (20330441)

Co-Investigator(Renkei-kenkyūsha) Yamamoto Satoshi  兵庫医療大学, 薬学部, 教授 (60220464)
Noguchi Koichi  兵庫医療大学, 医学部, 教授 (10212127)
Wang Shenglan  兵庫医療大学, 薬学部, 助教授 (50714359)
Kogure Yoko  兵庫医療大学, 薬学部, 助教授 (60548684)
Project Period (FY) 2014-04-01 – 2017-03-31
KeywordsAMPK / TRPA1 / Pain
Outline of Final Research Achievements

AMP activated protein kinase (AMPK) is a widely expressed intracellular energy sensor that monitors and modulates energy expenditure. AMPK is activated in response to ATP consumption, and upon activation, AMPK phosphorylates a broad range of downstream targets, which results in a reduction in energy usage and an increase in energy production. Transient receptor potential ankyrin 1 (TRPA1) channel is a widely recognized chemical and thermal sensor that plays vital roles in pain transduction.
Here, we discovered a functional link between AMPK and TRPA1 in dorsal root ganglion (DRG) neurons, in which AMPK activation rapidly inhibit TRPA1 channel activity within minutes. These observation demonstrated an important role and the molecular mechanism of AMPK in pain generation.

Free Research Field

Pain Research

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Published: 2018-03-22   Modified: 2018-04-03  

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