Gene-targeting reveals physiological roles and complex regulation of the phosphoinositide 3-kinases

被引：32

作者：

Foukas, LC

Okkenhaug, K ^{[1
]}

机构：

[1] Babraham Inst, Lab Lymphocyte Activat & Dev, Cambridge CB2 4AT, England

[2] Ludwig Inst Canc Res, London W1W 7BS, England

来源：

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS | 2003年 / 414卷 / 01期

关键词：

D O I：

10.1016/S0003-9861(03)00177-2

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Phosphoinositide 3-kinases (PI3Ks) are represented by a family of eight distinct enzymes that can be divided into three classes based on their structure and function. The class I PI3Ks are heterodimeric enzymes that are regulated by recruitment to plasma membrane following receptor activation and which control numerous cellular functions, including growth, differentiation, migration, survival, and metabolism. New light has been shed on the biological role of individual members of the class I PI3Ks and their regulatory subunits through gene-targeting experiments. In addition, these experiments have brought the complexity of how PI3K activation is regulated into focus. (C) 2003 Elsevier Science (USA). All rights reserved.

引用

收藏

页码：13 / 18

页数：6

相关论文

共 60 条

[1] Pten inactivation alters peripheral B lymphocyte fate and reconstitutes CD19 function [J].

Anzelon, AN ;

Wu, H ;

Rickert, RC .

NATURE IMMUNOLOGY, 2003, 4 (03) :287-294

[2] PHOSPHATIDYLINOSITOL 3'-KINASE IS ACTIVATED BY ASSOCIATION WITH IRS-1 DURING INSULIN STIMULATION [J].

BACKER, JM ;

MYERS, MG ;

SHOELSON, SE ;

CHIN, DJ ;

SUN, XJ ;

MIRALPEIX, M ;

HU, P ;

MARGOLIS, B ;

SKOLNIK, EY ;

SCHLESSINGER, J ;

WHITE, MF .

EMBO JOURNAL, 1992, 11 (09) :3469-3479

[3] Tumour biology - Weakening link to colorectal cancer? [J].

Barbier, M ;

Attoub, S ;

Calvez, R ;

Laffargue, M ;

Jarry, A ;

Mareel, M ;

Altruda, F ;

Gespach, C ;

Wu, D ;

Lu, B ;

Hirsch, E ;

Wymann, MP .

NATURE, 2001, 413 (6858) :796-796

[4] Comparison of the kinetic properties of the lipid- and protein-kinase activities of the p110α and p110β catalytic subunits of class-Ia phosphoinositide 3-kinases [J].

Beeton, CA ;

Chance, EM ;

Foukas, LC ;

Shepherd, PR .

BIOCHEMICAL JOURNAL, 2000, 350 :353-359

[5] Proliferative defect and embryonic lethality in mice homozygous for a deletion in the p110α subunit of phosphoinositide 3-kinase [J].

Bi, L ;

Okabe, I ;

Bernard, DJ ;

Wynshaw-Boris, A ;

Nussbaum, RL .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (16) :10963-10968

[6] Early embryonic lethality in mice deficient in the p110β catalytic subunit of PI 3-kinase [J].

Bi, L ;

Okabe, I ;

Bernard, DJ ;

Nussbaum, RL .

MAMMALIAN GENOME, 2002, 13 (03) :169-172

[7] New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase AKT pathway [J].

Cantley, LC ;

Neel, BG .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (08) :4240-4245

[8]

CARPENTER CL, 1993, J BIOL CHEM, V268, P9478

[9] Small GTPases and tyrosine kinases coregulate a molecular switch in the phosphoinositide 3-kinase regulatory subunit [J].

Chan, TO ;

Rodeck, U ;

Chan, AM ;

Kimmelman, AC ;

Rittenhouse, SE ;

Panayotou, G ;

Tsichlis, PN .

CANCER CELL, 2002, 1 (02) :181-191

[10] Phosphatidylinositol-3-OH kinases are Rab5 effectors [J].

Christoforidis, S ;

Miaczynska, M ;

Ashman, K ;

Wilm, M ;

Zhao, LY ;

Yip, SC ;

Waterfield, MD ;

Backer, JM ;

Zerial, M .

NATURE CELL BIOLOGY, 1999, 1 (04) :249-252

← 1 2 3 4 5 6 →