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学科主题: 基础医学
题名:
Activation of m1 muscarinic acetylcholine receptor induces surface transport of KCNQ channels through a CRMP-2-mediated pathway
作者: Jiang, Ling1,2,3; Kosenko, Anastasia3; Yu, Clinton4; Huang, Lan4; Li, Xuejun1,2; Hoshi, Naoto3,4
关键词: Channel trafficking ; Muscarinic acetylcholine receptor ; KCNQ2 ; CK2 ; GSK3 ; CRMP-2
刊名: JOURNAL OF CELL SCIENCE
发表日期: 2015-11-15
DOI: 10.1242/jcs.175547
卷: 128, 期:22, 页:4235-4245
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cell Biology
研究领域[WOS]: Cell Biology
关键词[WOS]: BULLFROG SYMPATHETIC NEURONS ; POTASSIUM CHANNELS ; K+ CHANNELS ; EXPRESSION ; PROTEIN ; CRMP-2 ; COMPLEX ; SUPPRESSION ; MICROSCOPY ; MEMBRANE
英文摘要:

Neuronal excitability is strictly regulated by various mechanisms, including modulation of ion channel activity and trafficking. Stimulation of m1 muscarinic acetylcholine receptor (also known as CHRM1) increases neuronal excitability by suppressing the M-current generated by the Kv7/KCNQ channel family. We found that m1 muscarinic acetylcholine receptor stimulation also triggers surface transport of KCNQ subunits. This receptor-induced surface transport was observed with KCNQ2 as well as KCNQ3 homomeric channels, but not with Kv3.1 channels. Deletion analyses identified that a conserved domain in a proximal region of the N-terminal tail of KCNQ protein is crucial for this surface transport - the translocation domain. Proteins that bind to this domain were identified as alpha-and beta-tubulin and collapsin response mediator protein 2 (CRMP-2; also known as DPYSL2). An inhibitor of casein kinase 2 (CK2) reduced tubulin binding to the translocation domain, whereas an inhibitor of glycogen synthase kinase 3 (GSK3) facilitated CRMP-2 binding to the translocation domain. Consistently, treatment with the GSK3 inhibitor enhanced receptor-induced KCNQ2 surface transport. M-current recordings from neurons showed that treatment with a GSK3 inhibitor shortened the duration of muscarinic suppression and led to over-recovery of the M-current. These results suggest that m1 muscarinic acetylcholine receptor stimulates surface transport of KCNQ channels through a CRMP-2-mediated pathway.

语种: 英语
所属项目编号: R01NS067288 ; R01GM074830 ; 81473235 ; 81020108031
项目资助者: National Institutes of Health ; National Natural Science Foundation of China
WOS记录号: WOS:000366314900021
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/66690
Appears in Collections:基础医学院_期刊论文

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作者单位: 1.Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, State Key Lab Nat & Biomimet Drugs,Dept Pharmacol, Beijing 100191, Peoples R China
2.Peking Univ, Beijing Key Lab Tumor Syst Biol, Beijing 100191, Peoples R China
3.Univ Calif Irvine, Dept Pharmacol, Irvine, CA 92617 USA
4.Univ Calif Irvine, Dept Physiol & Biophys, Irvine, CA 92697 USA

Recommended Citation:
Jiang, Ling,Kosenko, Anastasia,Yu, Clinton,et al. Activation of m1 muscarinic acetylcholine receptor induces surface transport of KCNQ channels through a CRMP-2-mediated pathway[J]. JOURNAL OF CELL SCIENCE,2015,128(22):4235-4245.
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