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学科主题临床医学
alpha(1A)-Adrenergic Receptor Induces Activation of Extracellular Signal-Regulated Kinase 1/2 through Endocytic Pathway
Liu, Fei1,2; He, Kangmin1,2; Yang, Xinxing3; Xu, Ning1,2; Liang, Zhangyi3; Xu, Ming1,2; Zhao, Xinsheng3; Han, Qide1,2; Zhang, Youyi1,2
刊名PLOS ONE
2011-06-28
DOI10.1371/journal.pone.0021520
6期:6
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
资助者National Key Basic Research Program of People&prime ; s Republic of China ; Natural Science Foundation of China ; National Key Basic Research Program of People&prime ; s Republic of China ; Natural Science Foundation of China
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]PROTEIN-KINASE ; MYOSIN-V ; ALPHA(1)-ADRENOCEPTOR SUBTYPES ; PHOSPHATIDYLINOSITOL 3-KINASE ; DEPENDENT ENDOCYTOSIS ; MEDIATED ENDOCYTOSIS ; CARDIAC-HYPERTROPHY ; TRANSGENIC MICE ; BETA-ARRESTINS ; CELLS
英文摘要

G protein-coupled receptors (GPCRs) activate mitogen-activated protein kinases through a number of distinct pathways in cells. Increasing evidence has suggested that endosomal signaling has an important role in receptor signal transduction. Here we investigated the involvement of endocytosis in alpha(1A)-adrenergic receptor (alpha(1A)-AR)-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Agonist-mediated endocytic traffic of alpha(1A)-AR was assessed by real-time imaging of living, stably transfected human embryonic kidney 293A cells (HEK-293A). alpha(1A)-AR was internalized dynamically in cells with agonist stimulation, and actin filaments regulated the initial trafficking of alpha(1A)-AR. alpha(1A)-AR-induced activation of ERK1/2 but not p38 MAPK was sensitive to disruption of endocytosis, as demonstrated by 4 degrees C chilling, dynamin mutation and treatment with cytochalasin D (actin depolymerizing agent). Activation of protein kinase C (PKC) and C-Raf by alpha(1A)-AR was not affected by 4 degrees C chilling or cytochalasin D treatment. U73122 (a phospholipase C [PLC] inhibitor) and Ro 31-8220 (a PKC inhibitor) inhibited alpha(1B)-AR-but not alpha(1A)-AR-induced ERK1/2 activation. These data suggest that the endocytic pathway is involved in a1A-AR-induced ERK1/2 activation, which is independent of G(q)/PLC/PKC signaling.

语种英语
所属项目编号2007CB935601 ; 2006CB910300 ; 81030001 ; 30821001 ; 20733001
资助者National Key Basic Research Program of People&prime ; s Republic of China ; Natural Science Foundation of China ; National Key Basic Research Program of People&prime ; s Republic of China ; Natural Science Foundation of China
WOS记录号WOS:000292142800031
引用统计
被引频次:11[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/400002259/56193
专题北京大学第三临床医学院_心血管内科
作者单位1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China
2.Peking Univ, Inst Vasc Med, Hosp 3, Beijing 100871, Peoples R China
3.Peking Univ, Beijing Natl Lab Mol Sci,Biodynam Opt Imaging Ctr, State Key Lab Struct Chem Unstable & Stable Speci, Dept Biol Chem,Coll Chem & Mol Engn, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Liu, Fei,He, Kangmin,Yang, Xinxing,et al. alpha(1A)-Adrenergic Receptor Induces Activation of Extracellular Signal-Regulated Kinase 1/2 through Endocytic Pathway[J]. PLOS ONE,2011,6(6).
APA Liu, Fei.,He, Kangmin.,Yang, Xinxing.,Xu, Ning.,Liang, Zhangyi.,...&Zhang, Youyi.(2011).alpha(1A)-Adrenergic Receptor Induces Activation of Extracellular Signal-Regulated Kinase 1/2 through Endocytic Pathway.PLOS ONE,6(6).
MLA Liu, Fei,et al."alpha(1A)-Adrenergic Receptor Induces Activation of Extracellular Signal-Regulated Kinase 1/2 through Endocytic Pathway".PLOS ONE 6.6(2011).
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