TRPA1 underlies a sensing mechanism for O2

被引：0

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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学科分类号：

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]

引用

页码：701 / 711

页数：10

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