IR@PKUHSC  > 北京大学第二临床医学院
学科主题临床医学
beta-Arrestin 2 regulates toll-like receptor 4-mediated apoptotic signalling through glycogen synthase kinase-3 beta
Li, Hui1,2; Sun, Xiuli1,3; LeSage, Gene1; Zhang, Yi1; Liang, Zhihou2; Chen, Jixiang2; Hanley, Gregory4; He, Lei1; Sun, Shenggang2; Yin, Deling1
关键词apoptosis beta-arrestin 2 glycogen synthase kinase-3 beta serum deprivation Toll-like receptor 4
刊名IMMUNOLOGY
2010-08-01
DOI10.1111/j.1365-2567.2010.03256.x
130期:4页:556-563
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Immunology
研究领域[WOS]Immunology
关键词[WOS]CELL-SURVIVAL ; ISCHEMIC-INJURY ; B-CELLS ; ACTIVATION ; LIPOPOLYSACCHARIDE ; KINASE ; PROTECTS ; COMPLEX ; STRESS ; GLYCOGEN-SYNTHASE-KINASE-3-BETA
英文摘要

P>Toll-like receptor 4 (TLR4), a key member of the TLR family, has been well characterized by its function in the induction of inflammatory products of innate immunity. However, the involvement of TLR4 in a variety of apoptotic events by an unknown mechanism has been the focus of great interest. Our investigation found that TLR4 promoted apoptotic signalling by affecting the glycogen synthase kinase-3 beta (GSK-3 beta) pathway in a serum-deprivation-induced apoptotic paradigm. Serum deprivation induces GSK-3 beta activation in a pathway that leads to subsequent cell apoptosis. Intriguingly, this apoptotic cascade is amplified in presence of TLR4 but greatly attenuated by beta-arrestin 2, another critical molecule implicated in TLR4-mediated immune responses. Our data suggest that the association of beta-arrestin 2 with GSK-3 beta contributes to the stabilization of phospho-GSK-3 beta, an inactive form of GSK-3 beta. It becomes a critical determinant for the attenuation of TLR4-initiated apoptosis by beta-arrestin 2. Taken together, we demonstrate that the TLR4 possesses the capability of accelerating GSK-3 beta activation thereby deteriorating serum-deprivation-induced apoptosis; beta-arrestin 2 represents an inhibitory effect on the TLR4-mediated apoptotic cascade, through controlling the homeostasis of activation and inactivation of GSK-3 beta.

语种英语
WOS记录号WOS:000279735800011
项目编号DA020120 ; 2-25491
资助机构National Institutes of Health (NIH) ; East Tennessee State University Research Development Committee (ETSU RDC)
引用统计
被引频次:22[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/400002259/58423
专题北京大学第二临床医学院
作者单位1.E Tennessee State Univ, Dept Internal Med, Coll Med, Johnson City, TN 37614 USA
2.Huazhong Univ Sci & Technol, Dept Neurol, Union Hosp, Tongji Med Coll, Wuhan 430022, Peoples R China
3.Peking Univ, Dept Obstet & Gynecol, Peoples Hosp, Beijing 100871, Peoples R China
4.E Tennessee State Univ, Coll Med, Lab Anim Resources, Johnson City, TN 37614 USA
推荐引用方式
GB/T 7714
Li, Hui,Sun, Xiuli,LeSage, Gene,et al. beta-Arrestin 2 regulates toll-like receptor 4-mediated apoptotic signalling through glycogen synthase kinase-3 beta[J]. IMMUNOLOGY,2010,130(4):556-563.
APA Li, Hui.,Sun, Xiuli.,LeSage, Gene.,Zhang, Yi.,Liang, Zhihou.,...&Yin, Deling.(2010).beta-Arrestin 2 regulates toll-like receptor 4-mediated apoptotic signalling through glycogen synthase kinase-3 beta.IMMUNOLOGY,130(4),556-563.
MLA Li, Hui,et al."beta-Arrestin 2 regulates toll-like receptor 4-mediated apoptotic signalling through glycogen synthase kinase-3 beta".IMMUNOLOGY 130.4(2010):556-563.
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