PTEN and myotubularin phosphatases: from 3-phosphoinositide dephosphorylation to disease

被引：146

作者：

Wishart, MJ ^{[1
]}

Dixon, JE ^{[1
]}

机构：

[1] Univ Michigan, Sch Med, Dept Biol Chem, Ann Arbor, MI 48109 USA

来源：

TRENDS IN CELL BIOLOGY | 2002年 / 12卷 / 12期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1016/S0962-8924(02)02412-1

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The phosphatase and tensin homolog deleted on chromosome ten (PTEN) and myotubularin (MTM1) represent subfamilies of protein tyrosine phosphatases whose principal physiological substrates are D3-phosphorylated inositol phospholipids. As lipid phosphatases, PTEN- and MTM1-related (MTMR) proteins dephosphorylate the products of phosphoinositide 3-kinases and antagonize downstream effectors that utilize 3-phosphoinositides as ligands for protein targeting domains or allosteric activation. Here, we describe the cellular mechanisms of PTEN and MTMR function and their role in the etiology of cancer and other human diseases.

引用

页码：579 / 585

页数：11

共 42 条

[1] Negative feedback regulation of the tumor suppressor PTEN by phosphoinositide-induced serine phosphorylation [J].

Birle, D ;

Bottini, N ;

Williams, S ;

Huynh, H ;

deBelle, I ;

Adamson, E ;

Mustelin, T .

JOURNAL OF IMMUNOLOGY, 2002, 169 (01) :286-291

[2] Charcot-Marie-Tooth type 4B is caused by mutations in the gene encoding myotubularin-related protein-2 [J].

Bolino, A ;

Muglia, M ;

Conforti, FL ;

LeGuern, E ;

Salih, MAM ;

Georgiou, DM ;

Christodoulou, K ;

Hausmanowa-Petrusewicz, I ;

Mandich, P ;

Schenone, A ;

Gambardella, A ;

Bono, F ;

Quattrone, A ;

Devoto, M ;

Monaco, AP .

NATURE GENETICS, 2000, 25 (01) :17-19

[3] Ten years of protein kinase B signalling: a hard Akt to follow [J].

Brazil, DP ;

Hemmings, BA .

TRENDS IN BIOCHEMICAL SCIENCES, 2001, 26 (11) :657-664

[4] Specific inhibition of PTEN expression reverses hyperglycemia in diabetic mice [J].

Butler, M ;

McKay, RA ;

Popoff, IJ ;

Gaarde, WA ;

Witchell, D ;

Murray, SF ;

Dean, NM ;

Bhanot, S ;

Monia, BP .

DIABETES, 2002, 51 (04) :1028-1034

[5] Regulation of myocardial contractility and cell size by distinct PI3K-PTEN signaling pathways [J].

Crackower, MA ;

Oudit, GY ;

Kozieradzki, I ;

Sarao, R ;

Sun, H ;

Sasaki, T ;

Hirsch, E ;

Suzuki, A ;

Shioi, T ;

Irie-Sasaki, J ;

Sah, R ;

Cheng, HYM ;

Rybin, VO ;

Lembo, G ;

Fratta, L ;

Oliveira-dos-Santos, AJ ;

Benovic, JL ;

Kahn, CR ;

Izumo, S ;

Steinberg, SF ;

Wymann, MP ;

Backx, PH ;

Penninger, JM .

CELL, 2002, 110 (06) :737-749

[6] Modular phosphoinositide-binding domains - their role in signalling and membrane trafficking [J].

Cullen, PJ ;

Cozier, GE ;

Banting, G ;

Mellor, H .

CURRENT BIOLOGY, 2001, 11 (21) :R882-R893

[7] Pten is essential for embryonic development and tumour suppression [J].

Di Cristofano, A ;

Pesce, B ;

Cordon-Cardo, C ;

Pandolfi, PP .

NATURE GENETICS, 1998, 19 (04) :348-355

[8]

Firestein R, 2002, J CLIN INVEST, V109, P1165, DOI [10.1172/JCI200212589, 10.1172/JCI0212589]

[9] Spatial and temporal regulation of 3-phosphoinositides by PI 3-kinase and PTEN mediates chemotaxis [J].

Funamoto, S ;

Meili, R ;

Lee, S ;

Parry, L ;

Firtel, RA .

CELL, 2002, 109 (05) :611-623

[10] Drosophila tumor suppressor PTEN controls cell size and number by antagonizing the Chico/PI3-kinase signaling pathway [J].

Goberdhan, DCI ;

Paricio, N ;

Goodman, EC ;

Mlodzik, M ;

Wilson, C .

GENES & DEVELOPMENT, 1999, 13 (24) :3244-3258

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