TRPA1 underlies a sensing mechanism for O2

被引:0
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作者
Nobuaki Takahashi
Tomoyuki Kuwaki
Shigeki Kiyonaka
Tomohiro Numata
Daisuke Kozai
Yusuke Mizuno
Shinichiro Yamamoto
Shinji Naito
Ellen Knevels
Peter Carmeliet
Toru Oga
Shuji Kaneko
Seiji Suga
Toshiki Nokami
Jun-ichi Yoshida
Yasuo Mori
机构
[1] Graduate School of Engineering,Department of Synthetic Chemistry and Biological Chemistry
[2] Kyoto University,Department of Technology and Ecology
[3] Hall of Global Environmental Studies,Department of Physiology
[4] Kyoto University,Division of Pathology
[5] Advanced Biomedical Engineering Research Unit,Department of Respiratory Care and Sleep Control Medicine
[6] Kyoto University,Department of Molecular Pharmacology
[7] Graduate School of Medical and Dental Sciences,undefined
[8] Kagoshima University,undefined
[9] Core Research for Evolutional Science and Technology,undefined
[10] Japan Science and Technology Agency,undefined
[11] National Ureshino Hospital,undefined
[12] Vesalius Research Center,undefined
[13] Catholic University of Leuven,undefined
[14] Vesalius Research Center,undefined
[15] Flanders Institute for Biotechnology,undefined
[16] Graduate School of Medicine,undefined
[17] Kyoto University,undefined
[18] Graduate School of Pharmaceutical Sciences,undefined
[19] Kyoto University,undefined
来源
Nature Chemical Biology | 2011年 / 7卷
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摘要
The redox-sensitive TRP channel TRPA1 is activated in hyperoxic and hypoxic conditions directly through modification of cysteine residues by O2 and indirectly through prolyl hydroxylation by PHDs, enzymes related to the hypoxia-inducible factor HIF-1, thus helping to explain how O2 is sensed by sensory and vagal neurons.[graphic not available: see fulltext]
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页码:701 / 711
页数:10
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