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学科主题临床医学
14-3-3 Proteins regulate glycogen synthase 3 beta phosphorylation and inhibit cardiomyocyte hypertrophy
Liao, WQ; Wang, SY; Han, CD; Zhang, YY
关键词14-3-3 Proteins Cardiomyocyte Hypertrophy Nfat Pkb/gsk3 Beta
刊名FEBS JOURNAL
2005-04-01
DOI10.1111/j.1742-4658.2005.04614.x
272期:8页:1845-1854
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]14-3-3 PROTEINS ; AMPHIPATHIC GROOVE ; SIGNAL ; APOPTOSIS ; BINDS ; DISSOCIATION ; ACTIVATION ; KINASE-1 ; PEPTIDE ; SYSTEM
英文摘要

14-3-3 Proteins are dimeric phophoserine-binding molecules that participate in important cellular processes such as cell proliferation, cell-cycle control and the stress response. In this work, we report that several isoforms of 14-3-3s are expressed in neonatal rat cardiomyocytes. To understand their function, we utilized a general 14-3-3 peptide inhibitor, R18, to disrupt 14-3-3 functions in cardiomyocytes. Cardiomyocytes infected with adenovirus-expressing YFP-R18 (AdR18) exhibited markedly increased protein synthesis and atrial natriuretic peptide production and potentiated the responses to norepinephrine stimulation. This response was blocked by the pretreatment with LY294002, a phosphoinositide 3-kinase (PI3K) inhibitor. Consistent with a role of PI3K in the R18 effect, R18 induced phosphorylation of a protein cloned from the vakt oncogene of retrovirus AKT8 (Akt - also called protein kinase B, PKB) at Ser473 and glycogen synthase 3 beta (GSK3 beta) at Ser9, but not extracellular signal-regulated kinase 1/2 (ERK1/2). AdR18-induced PKB and GSK3 beta phosphorylation was completely blocked by LY294002. In addition, a member of the nuclear factor of activated T cells (NFAT) family, NFAT3, was converted into faster mobility forms and translocated into the nucleus upon the treatment of AdR18. These results suggest that 14-3-3s inhibits cardiomyocytes hypertrophy through regulation of the PI3K/PKB/GSK3 beta and NFAT pathway.

语种英语
WOS记录号WOS:000228266700003
引用统计
被引频次:37[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/400002259/54759
专题北京大学第三临床医学院_心血管内科
作者单位1.Peking Univ, Third Hosp, Inst Vasc Med, Beijing 100083, Peoples R China
2.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100083, Peoples R China
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GB/T 7714
Liao, WQ,Wang, SY,Han, CD,et al. 14-3-3 Proteins regulate glycogen synthase 3 beta phosphorylation and inhibit cardiomyocyte hypertrophy[J]. FEBS JOURNAL,2005,272(8):1845-1854.
APA Liao, WQ,Wang, SY,Han, CD,&Zhang, YY.(2005).14-3-3 Proteins regulate glycogen synthase 3 beta phosphorylation and inhibit cardiomyocyte hypertrophy.FEBS JOURNAL,272(8),1845-1854.
MLA Liao, WQ,et al."14-3-3 Proteins regulate glycogen synthase 3 beta phosphorylation and inhibit cardiomyocyte hypertrophy".FEBS JOURNAL 272.8(2005):1845-1854.
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