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学科主题: 药学
题名:
Divalent cations potentiate TRPV1 channel by lowering the heat activation threshold
作者: Cao, Xu1,2; Ma, Linlin2,3; Yang, Fan2; Wang, KeWei1,4; Zheng, Jie2
刊名: JOURNAL OF GENERAL PHYSIOLOGY
发表日期: 2014
DOI: 10.1085/jgp.201311025
卷: 143, 期:1, 页:75-90
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Physiology
研究领域[WOS]: Physiology
关键词[WOS]: CAPSAICIN RECEPTOR TRPV1 ; EXTERNAL PROTONATION SITES ; 2 INACTIVATION MECHANISMS ; ROOT GANGLION NEURONS ; POTASSIUM CHANNELS ; ION-CHANNEL ; K+ CHANNEL ; VANILLOID RECEPTOR-1 ; PROTEIN-KINASE ; PORE TURRET
英文摘要:

Transient receptor potential vanilloid type 1 (TRPV1) channel responds to a wide spectrum of physical and chemical stimuli. In doing so, it serves as a polymodal cellular sensor for temperature change and pain. Many chemicals are known to strongly potentiate TRPV1 activation, though how this is achieved remains unclear. In this study we investigated the molecular mechanism underlying the gating effects of divalent cations Mg2+ and Ba2+. Using a combination of fluorescence imaging and patch-clamp analysis, we found that these cations potentiate TRPV1 gating by most likely promoting the heat activation process. Mg2+ substantially lowers the activation threshold temperature; as a result, a significant fraction of channels are heat-activated at room temperature. Although Mg2+ also potentiates capsaicin- nd voltage-dependent activation, these processes were found either to be not required (in the case of capsaicin) or insufficient (in the case of voltage) to mediate the activating effect. In support of a selective effect on heat activation, Mg2+ and Ba2+ cause a Ca2+-independent desensitization that specifically prevents heat-induced channel activation but does not prevent capsaicin-induced activation. These results can be satisfactorily explained within an allosteric gating framework in which divalent cations strongly promote the heat-dependent conformational change or its coupling to channel activation, which is further coupled to the voltage-and capsaicin-dependent processes.

语种: 英语
所属项目编号: R01NS072377 ; B07001 ; 2013CB531302 ; 81221002 ; APP1035102 ; 10PRE4170142
项目资助者: National Institutes of Health ; UC Davis Health System Research Award ; Ministry of Education of China 111 Project ; Ministry of Science and Technology of China ; National Science Foundation of China ; Australian National Health and Medical Research Council fellowship ; American Heart Association predoctoral fellowship
WOS记录号: WOS:000329129800011
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63656
Appears in Collections:北京大学药学院_期刊论文

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作者单位: 1.Peking Univ, Sch Pharmaceut Sci, Dept Mol & Cellular Pharmacol, State Key Lab Nat & Biomimet Drugs, Beijing 100191, Peoples R China
2.Univ Calif Davis, Sch Med, Dept Physiol & Membrane Biol, Davis, CA 95616 USA
3.Univ Queensland, Inst Mol Biosci, St Lucia, Qld 4072, Australia
4.Peking Univ, IDG McGovern Inst Brain Res, Beijing 100871, Peoples R China

Recommended Citation:
Cao, Xu,Ma, Linlin,Yang, Fan,et al. Divalent cations potentiate TRPV1 channel by lowering the heat activation threshold[J]. JOURNAL OF GENERAL PHYSIOLOGY,2014,143(1):75-90.
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