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|本期目录/Table of Contents|

蛋白磷酸酶PHLPP对Akt通路的抑制作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2012年第2期
页码:
263-266
栏目:
综述
出版日期:
2012-04-25

文章信息/Info

Title:
Suppression of Akt pathway by protein phosphatase PHLPP
作者:
吴伟强1; 殷 玥2综述; 马 恒2审校
(第四军医大学：1.学员17队，2.生理学教研室，陕西 西安 710032)
Author(s):
WU Wei-qiang1;  YIN Yue2;  MA Heng2
(1.17th Cadet Battalion, 2.Department of Physiology, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
蛋白激酶B; PHLPP; 肿瘤; 糖尿病; 缺血/再灌注
Keywords:
Akt;  PHLPP;  tumor;  diabetes;  ischemia/reperfusion
分类号:
Q555.7
DOI:
-
文献标识码:
A
摘要:
近年发现的蛋白磷酸酶PHLPP日益得到重视。PHLPP能够特异性地使蛋白激酶B（Akt）发生去磷酸化并抑制其活性，进而参与细胞生理功能的调控。PHLPP与肿瘤、糖尿病及心肌缺血/再灌注损伤等疾病的发生发展也有密切关系。
Abstract:
As a novel protein phosphatase, PHLPP specifically induces dephosphorylation of protein kinase B (Akt) that inhibits Akt activity. The role of PHLPP in cell physiological regulation has led to increasing attention to this process. The close relationship with the onset of tumors, diabetes and myocardial ischemia/reperfusion injury all highlight the important biological function of PHLPP.

参考文献/References

[1]Liao Y,Hung MC.Physiological regulation of Akt activity and stability[J].Am J Transl Res,2010,2(1):19-42.

[2]Qiao M,Iglehart JD,Pardee AB.Metastatic potential of 21T human breast cancer cells depends on Akt/protein kinase B activation[J].Cancer Res,2007,67(11):5293-5299.

[3]Aviv Y,Kirshenbaum LA.Kirshenbaum.Novel phosphatase PHLPP-1 regulates mitochondrial Akt activity and cardiac cell survival[J].Circ Res,2010,107(4):448-450.

[4] Hirano I,Nakamura S,Yokota D,et al.Depletion of Pleckstrin homology domain leucine-rich repeat protein phosphatases 1 and 2 by Bcr-Abl promotes chronic myelogenous leukemia cell proliferation through continuous phosphorylation of Akt isoforms[J].J Biol Chem,2009,284(33):22155-22165.

[5]Siddall HK,Warrell CE,Yellon DM,et al.Ischemia-reperfusion injury and cardioprotection: investigating PTEN, the phosphatase that negatively regulates PI3K, using a congenital model of PTEN haploinsufficiency[J].Basic Res Cardiol,2008,103(6):560-568.

[6]Brognard J,Newton AC.PHLiPPing the switch on Akt and protein kinase C signaling[J].Trends Endocrinol Metab,2008,19(6):223-230.

[7]Brognard J,Sierecki E,Gao T,et al.PHLPP and a second isoform, PHLPP2, differentially attenuate the amplitude of Akt signaling by regulating distinct Akt isoforms[J].Mol Cell,2007,25(6):917-931.

[8]doza MC,Blenis J.PHLPPing it off:phosphatases get in the Akt[J].Mol Cell,2007,25(6):798-800.

[9]Cozzone D,Fr jd S, Disse E,et al.Isoform-specific defects of insulin stimulation of Akt/protein kinase B (PKB) in skeletal muscle cells from type 2 diabetic patients[J].Diabetologia,2008,51(3):512-521.

[10]张卫卫,刘 艳,师堂旺,等.DIDS通过PI3-K/Akt途径减弱缺血/再灌注损伤诱导心肌细胞凋亡[J].心脏杂志,2009,21(3):313-316.

[11]Miyamoto S,Purcell NH,Smith JM,et al.PHLPP-1 negatively regulates Akt activity and survival in the heart[J].Circ Res,2010,107(4):476-484.

备注/Memo

备注/Memo:
收稿日期：2011-06-27.通讯作者：马恒，副教授，主要从事心肌内源性保护机制研究 Email：hengma@fmmu.edu.cn 作者简介：吴伟强，本科生 Email：3032008072@fmmu.edu.cn 共同第一作者：殷玥，实验员 Email：music1021@126.com
更新日期/Last Update: 2012-04-01