INT117601
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Structurally unrelated cysteine-modifying agents such as iodoacetamide (IA) and (2-aminoethyl)methanethiosulphonate (MTSEA) also bind and activate TRPA1. | |||||||||||||||
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Noxious compounds activate TRPA1 ion channels through covalent modification of cysteines. | |||||||||||||||
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TRPA1 is activated by a variety of noxious stimuli, including cold temperatures, pungent natural compounds, and environmental irritants. | |||||||||||||||
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How such diverse stimuli activate TRPA1 is not known. | |||||||||||||||
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In excised patches, reactive compounds activated TRPA1 currents that were maintained at least 10 min after washout of the compound in calcium-free solutions. | |||||||||||||||
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TRPA1, a TRP ion channel expressed in chemosensory C-fibers, is activated by almost all oxidizing and electrophilic chemicals, including chlorine, acrolein, tear gas agents, and methyl isocyanate, the highly noxious chemical released in the Bhopal disaster. | |||||||||||||||
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Chemicals likely activate TRPA1 through covalent protein modification. | |||||||||||||||
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TRPA1 antagonists camphor and gadolinium, and a general TRP blocker ruthenium red inhibited TRPA1 activation by acetaldehyde. | |||||||||||||||
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Combined with the lack of clear evidence of direct mechanical activation of the recombinant mammalian TRPA1, these data raise the possibility that TRPA1 is not intrinsically mechanically sensitive, but instead serves as an amplifier or a signal integrator that is downstream of the bona fide mechanoreceptor(s). | |||||||||||||||
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Cysteine-reducing agents suppressed H(2)O(2)-induced TRPA1 activation, whereas cysteine-oxidizing agents activated TRPA1. | |||||||||||||||
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Cysteine-reducing agents suppressed H(2)O(2)-induced TRPA1 activation, whereas cysteine-oxidizing agents activated TRPA1. | |||||||||||||||
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H(2)O(2) activated mouse TRPA1 to induce Ca(2+) influx and elicit non-selective cation currents. | |||||||||||||||
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Pronociceptive response elicited by TRPA1 receptor activation in mice. | |||||||||||||||
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Collectively, the present findings demonstrate that the TRPA1 agonist allyl isothiocyanate produces a consistent nociceptive response when injected into the mouse paw, an effect that seems to be mediated via activation of TRPA1 receptor and dependent on the capsaicin-sensitive fibers, release of histamine by mast cells and participation of tachykinins. | |||||||||||||||
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We further show that phospholipase C is an important signaling component for TRPA1 activation. | |||||||||||||||
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Collectively, these data demonstrate that TRPA1 activation elicits a painful sensation and provide a potential molecular model for why noxious cold can paradoxically be perceived as burning pain. | |||||||||||||||
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We show that, in addition to noxious cold, pungent natural compounds present in cinnamon oil, wintergreen oil, clove oil, mustard oil, and ginger all activate TRPA1 (ANKTM1). | |||||||||||||||
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We show that, in addition to noxious cold, pungent natural compounds present in cinnamon oil, wintergreen oil, clove oil, mustard oil, and ginger all activate TRPA1 (ANKTM1). | |||||||||||||||
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Heavy metals zinc, cadmium, and copper stimulate pulmonary sensory neurons via direct activation of TRPA1. | |||||||||||||||
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In summary, our results suggest that activation of TRPA1 in pulmonary C-fiber sensory nerves may contribute to the respiratory toxicity induced by airway exposure to these three heavy metals. | |||||||||||||||
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General Comments
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