Journal
NATURE CHEMICAL BIOLOGY
Volume 5, Issue 3, Pages 183-190Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nchembio.146
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Funding
- NIDCR NIH HHS [R01 DE016927-03, R01 DE016927, R01 DE016927-02, R01 DE016927-01A1] Funding Source: Medline
- NINDS NIH HHS [R01 NS046303-06, P30 NS045758-05S19003, R21 NS056942, R01 NS046303-04, P30 NS045758, R01 NS046303-05, R21 NS056942-01, R01 NS046303] Funding Source: Medline
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [R01DE016927] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P30NS045758, R21NS056942, R01NS046303] Funding Source: NIH RePORTER
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Zinc is an essential biological trace element. It is required for the structure or function of over 300 proteins, and it is increasingly recognized for its role in cell signaling. However, high concentrations of zinc have cytotoxic effects, and overexposure to zinc can cause pain and inflammation through unknown mechanisms. Here we show that zinc excites nociceptive somatosensory neurons and causes nociception in mice through TRPA1, a cation channel previously shown to mediate the pungency of wasabi and cinnamon through cysteine modification. Zinc activates TRPA1 through a unique mechanism that requires zinc influx through TRPA1 channels and subsequent activation via specific intracellular cysteine and histidine residues. TRPA1 is highly sensitive to intracellular zinc, as low nanomolar concentrations activate TRPA1 and modulate its sensitivity. These findings identify TRPA1 as an important target for the sensory effects of zinc and support an emerging role for zinc as a signaling molecule that can modulate sensory transmission.
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