IR@PKUHSC  > 北京大学第三临床医学院  > 超声影像科
学科主题基础医学
Activation of m1 muscarinic acetylcholine receptor induces surface transport of KCNQ channels through a CRMP-2-mediated pathway
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
2015-11-15
DOI10.1242/jcs.175547
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
WOS记录号WOS:000366314900021
项目编号R01NS067288 ; R01GM074830 ; 81473235 ; 81020108031
资助机构National Institutes of Health ; National Natural Science Foundation of China
引用统计
被引频次:2[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/66690
专题北京大学第三临床医学院_超声影像科
北京大学基础医学院
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
推荐引用方式
GB/T 7714
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.
APA Jiang, Ling,Kosenko, Anastasia,Yu, Clinton,Huang, Lan,Li, Xuejun,&Hoshi, Naoto.(2015).Activation of m1 muscarinic acetylcholine receptor induces surface transport of KCNQ channels through a CRMP-2-mediated pathway.JOURNAL OF CELL SCIENCE,128(22),4235-4245.
MLA Jiang, Ling,et al."Activation of m1 muscarinic acetylcholine receptor induces surface transport of KCNQ channels through a CRMP-2-mediated pathway".JOURNAL OF CELL SCIENCE 128.22(2015):4235-4245.
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