Signalling hypoxia by HIF hydroxylases

被引：296

作者：

Schofield, CJ

Ratcliffe, PJ

机构：

[1] Henry Wellcome Bldg Mol Physiol, Oxford OX3 7BN, England

[2] Oxford Ctr Mol Sci, Dept Chem, Oxford OX1 3TA, England

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2005年 / 338卷 / 01期

基金：

英国生物技术与生命科学研究理事会; 英国惠康基金;

关键词：

oxygenase; signalling; oxygen; iron; hypoxia inducible factor; transcription;

D O I：

10.1016/j.bbrc.2005.08.111

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：

Analysis of oxygen sensitive pathways that regulate the hypoxia inducible factor (HIF) transcriptional system has revealed a novel role for oxygenases in signalling hypoxia. The enzymes, which catalyse hydroxylation of specific prolyl and asparaginyl residues in the regulatory HIF-alpha subunits, belong to the superfamily of non-haem Fe(II)-dependent oxygenases that use the citric acid cycle intermediate 2-oxoglutarate (2OG) as a co-substrate. We review biochemical and physiological data that demonstrate a central role for these oxygenases in integrating multiple signals that coordinate cellular responses to hypoxia. (c) 2005 Elsevier Inc. All rights reserved.

引用

收藏

页码：617 / 626

页数：10

相关论文

共 66 条

[1] Differential function of the prolyl hydroxylases PHD1, PHD2, and PHD3 in the regulation of hypoxia-inducible factor [J].

Appelhoff, RJ ;

Tian, YM ;

Raval, RR ;

Turley, H ;

Harris, AL ;

Pugh, CW ;

Ratcliffe, PJ ;

Gleadle, JM .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (37) :38458-38465

[2] OS-9 interacts with hypoxia-inducible factor 1α and prolyl hydroxylases to promote oxygen-dependent degradation of HIF-1α [J].

Baek, JH ;

Mahon, PC ;

Oh, J ;

Kelly, B ;

Krishnamachary, B ;

Pearson, M ;

Chan, DA ;

Giaccia, AJ ;

Semenza, GL .

MOLECULAR CELL, 2005, 17 (04) :503-512

[3] Ascorbate metabolism and its regulation in animals [J].

Banhegyi, G ;

Braun, L ;

Csala, M ;

Puskas, F ;

Mandl, J .

FREE RADICAL BIOLOGY AND MEDICINE, 1997, 23 (05) :793-803

[4] HIF prolyl-hydroxylase 2 is the key oxygen sensor setting low steady-state levels of HIF-1α in normoxia [J].

Berra, E ;

Benizri, E ;

Ginouvès, A ;

Volmat, V ;

Roux, D ;

Pouysségur, J .

EMBO JOURNAL, 2003, 22 (16) :4082-4090

[5] HIF-1-dependent transcriptional activity is required for oxygen-mediated HIF-1α degradation [J].

Berra, E ;

Richard, DE ;

Gothié, E ;

Pouysségur, J .

FEBS LETTERS, 2001, 491 (1-2) :85-90

[6]

BILTON R, 2005, IN PRESS J BIOL CHEM, P1

[7] Oxygen sensing requires mitochondrial ROS but not oxidative phosphorylation [J].

Brunelle, JK ;

Bell, EL ;

Quesada, NM ;

Vercauteren, K ;

Tiranti, V ;

Zeviani, M ;

Scarpulla, RC ;

Chandel, NS .

CELL METABOLISM, 2005, 1 (06) :409-414

[8] Role of prolyl hydroxylation in oncogenically stabilized hypoxia-inducible factor-1α [J].

Chan, DA ;

Sutphin, PD ;

Denko, NC ;

Giaccia, AJ .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (42) :40112-40117

[9] Mitochondrial reactive oxygen species trigger hypoxia-induced transcription [J].

Chandel, NS ;

Maltepe, E ;

Goldwasser, E ;

Mathieu, CE ;

Simon, MC ;

Schumacker, PT .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (20) :11715-11720

[10] Dioxygen activation at mononuclear nonheme iron active sites: Enzymes, models, and intermediates [J].

Costas, M ;

Mehn, MP ;

Jensen, MP ;

Que, L .

CHEMICAL REVIEWS, 2004, 104 (02) :939-986

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