An ion channel essential for sensing chemical damage.

@article{citeulike:3008422, abstract = {Tissue damage and its downstream consequences are experimentally assayed by formaldehyde application, which indiscriminately modifies proteins and is presumed to cause pain through broadly acting mechanisms. Here we show that formaldehyde activates the ion channel TRPA1 and that TRPA1-deficient mice exhibit dramatically reduced formaldehyde-induced pain responses. 4-Hydroxynonenal, a reactive chemical produced endogenously during oxidative stress, and other related aldehydes also activate TRPA1 in vitro. Furthermore, painful responses to iodoacetamide, a nonspecific cysteine-alkylating compound, are abolished in TRPA1-deficient mice. Therefore, although these reactive chemicals modify many proteins, the associated pain appears mainly dependent on a single ion channel.}, address = {Department of Cell Biology, The Scripps Research Institute, La Jolla, California 92037, USA.}, author = {Macpherson, L. J. and Xiao, B. and Kwan, K. Y. and Petrus, M. J. and Dubin, A. E. and Hwang, S. and Cravatt, B. and Corey, D. P. and Patapoutian, A. }, citeulike-article-id = {3008422}, doi = {10.1523/JNEUROSCI.3600-07.2007}, issn = {1529-2401}, journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience}, keywords = {chemicals, irritants, trpa1}, month = {October}, number = {42}, pages = {11412--11415}, posted-at = {2008-07-16 14:00:39}, priority = {3}, title = {An ion channel essential for sensing chemical damage.}, url = {http://dx.doi.org/10.1523/JNEUROSCI.3600-07.2007}, volume = {27}, year = {2007} }

TY - JOUR ID - citeulike:3008422 L3 - citeulike-article-id:3008422 TI - An ion channel essential for sensing chemical damage. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience VL - 27 IS - 42 SP - 11412 EP - 11415 AD - Department of Cell Biology, The Scripps Research Institute, La Jolla, California 92037, USA. SN - 1529-2401 N2 - Tissue damage and its downstream consequences are experimentally assayed by formaldehyde application, which indiscriminately modifies proteins and is presumed to cause pain through broadly acting mechanisms. Here we show that formaldehyde activates the ion channel TRPA1 and that TRPA1-deficient mice exhibit dramatically reduced formaldehyde-induced pain responses. 4-Hydroxynonenal, a reactive chemical produced endogenously during oxidative stress, and other related aldehydes also activate TRPA1 in vitro. Furthermore, painful responses to iodoacetamide, a nonspecific cysteine-alkylating compound, are abolished in TRPA1-deficient mice. Therefore, although these reactive chemicals modify many proteins, the associated pain appears mainly dependent on a single ion channel. KW - chemicals KW - irritants KW - trpa1 AU - Macpherson, LJ AU - Xiao, B AU - Kwan, KY AU - Petrus, MJ AU - Dubin, AE AU - Hwang, S AU - Cravatt, B AU - Corey, DP AU - Patapoutian, A PY - 2007/10/17/ UR - http://dx.doi.org/10.1523/JNEUROSCI.3600-07.2007 ER -