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学科主题基础医学
Auxiliary KChIP4a Suppresses A-type K+ Current through Endoplasmic Reticulum (ER) Retention and Promoting Closed-state Inactivation of Kv4 Channels
Tang, Yi-Quan1; Liang, Ping1; Zhou, Jingheng1; Lu, Yanxin1; Lei, Lei1; Bian, Xiling1; Wang, KeWei1,2,3
刊名JOURNAL OF BIOLOGICAL CHEMISTRY
2013-05-24
DOI10.1074/jbc.M113.466052
288期:21页:14727-14741
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]TEMPORAL-LOBE EPILEPSY ; POTASSIUM CHANNELS ; ALPHA-SUBUNITS ; SURFACE EXPRESSION ; PYRAMIDAL NEURONS ; CARDIAC REPOLARIZATION ; TERMINAL DOMAINS ; STRUCTURAL BASIS ; TRAFFICKING ; PROTEIN
英文摘要

In the brain and heart, auxiliary Kv channel-interacting proteins (KChIPs) co-assemble with pore-forming Kv4 alpha-subunits to form a native K+ channel complex and regulate the expression and gating properties of Kv4 currents. Among the KChIP1-4 members, KChIP4a exhibits a unique N terminus that is known to suppress Kv4 function, but the underlying mechanism of Kv4 inhibition remains unknown. Using a combination of confocal imaging, surface biotinylation, and electrophysiological recordings, we identified a novel endoplasmic reticulum (ER) retention motif, consisting of six hydrophobic and aliphatic residues, 12-17 (LIVIVL), within the KChIP4a N-terminal KID, that functions to reduce surface expression of Kv4-KChIP complexes. This ER retention capacity is transferable and depends on its flanking location. In addition, adjacent to the ER retention motif, the residues 19-21 (VKL motif) directly promote closed-state inactivation of Kv4.3, thus leading to an inhibition of channel current. Taken together, our findings demonstrate that KChIP4a suppresses A-type Kv4 current via ER retention and enhancement of Kv4 closed-state inactivation.

语种英语
WOS记录号WOS:000319452100007
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被引频次:7[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/53066
专题北京大学基础医学院_神经生物学系
北京大学药学院_分子与细胞药理学系
北京大学临床肿瘤学院_肝胆胰外二科
北京大学临床肿瘤学院_妇科肿瘤科
作者单位1.Peking Univ, Dept Neurobiol, Neurosci Res Inst, Hlth Sci Ctr, Beijing 100191, Peoples R China
2.Peking Univ, Dept Mol & Cellular Pharmacol, State Key Lab Nat & Biomimet Drugs, Sch Pharmaceut Sci, Beijing 100191, Peoples R China
3.Peking Univ, Peking Univ Int Data Grp McGovern Inst Brain Res, Beijing 100871, Peoples R China
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Tang, Yi-Quan,Liang, Ping,Zhou, Jingheng,et al. Auxiliary KChIP4a Suppresses A-type K+ Current through Endoplasmic Reticulum (ER) Retention and Promoting Closed-state Inactivation of Kv4 Channels[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2013,288(21):14727-14741.
APA Tang, Yi-Quan.,Liang, Ping.,Zhou, Jingheng.,Lu, Yanxin.,Lei, Lei.,...&Wang, KeWei.(2013).Auxiliary KChIP4a Suppresses A-type K+ Current through Endoplasmic Reticulum (ER) Retention and Promoting Closed-state Inactivation of Kv4 Channels.JOURNAL OF BIOLOGICAL CHEMISTRY,288(21),14727-14741.
MLA Tang, Yi-Quan,et al."Auxiliary KChIP4a Suppresses A-type K+ Current through Endoplasmic Reticulum (ER) Retention and Promoting Closed-state Inactivation of Kv4 Channels".JOURNAL OF BIOLOGICAL CHEMISTRY 288.21(2013):14727-14741.
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