Receptor-targeting mechanisms of pain-causing toxins: How ow?

Receptor-targeting mechanisms of pain-causing toxins: How ow?
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DOI:
10.1016/j.toxicon.2012.04.336
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发表时间:
2012-09-01
期刊:
影响因子:
2.8
通讯作者:
Julius, David
Julius, David
中科院分区:
医学4区
文献类型:
--
作者:
Bohlen, Christopher J.;Julius, David

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毒液通常针对重要的过程,导致瘫痪或死亡,但许多类型的毒液也会引起强烈的疼痛。虽然这些产生疼痛的作用可能是全身性组织创伤的副产品,但现在有多个毒液衍生毒素的例子,它们靶向躯体感觉神经末梢,以激活伤害性(疼痛感测)神经通路。有趣的是,负责唤起疼痛的毒液成分的调查揭示了新的角色和/或配置的充分研究的毒素基序。这篇综述旨在突出针对辣椒素受体TRPV 1或酸敏感离子通道家族成员的疼痛产生毒素,并讨论毒液衍生的多价和多聚体复合物的效用。
Venoms often target vital processes to cause paralysis or death, but many types of venom also elicit notoriously intense pain. While these pain-producing effects can result as a byproduct of generalized tissue trauma, there are now multiple examples of venom-derived toxins that target somatosensory nerve terminals in order to activate nociceptive (pain-sensing) neural pathways. Intriguingly, investigation of the venom components that are responsible for evoking pain has revealed novel roles and/or configurations of well-studied toxin motifs. This review serves to highlight pain-producing toxins that target the capsaicin receptor, TRPV1, or members of the acid-sensing ion channel family, and to discuss the utility of venom-derived multivalent and multimeric complexes.
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