Nitric oxide signaling specificity - the heart of the problem

被引：112

作者：

Bredt, DS ^{[1
]}

机构：

[1] Univ Calif San Francisco, Sch Med, Dept Physiol, San Francisco, CA 94143 USA

来源：

JOURNAL OF CELL SCIENCE | 2003年 / 116卷 / 01期

关键词：

nitric oxide; heart; protein targeting; PDZ domain;

D O I：

10.1242/jcs.00183

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Nitric oxide (NO) is a gaseous free radical that functions as an endogenous mediator in numerous tissues. Because NO is both reactive and highly diffusible, its formation must be tightly regulated to control its synthesis and to specify its signaling. Indeed, molecular studies of the NO synthase (NOS) family of enzymes have elaborated a variety of mechanisms, including protein interactions, lipid modifications and protein phosphorylation cascades that spatially and temporally control NO biosynthesis. These mechanisms determine both the upstream cellular signals that stimulate NO formation and the downstream molecular targets for NO. Understanding these cellular pathways that control NOS will help us to elucidate the functional roles of NO and provide novel strategies to treat diseases associated with NO abnormalities.

引用

页码：9 / 15

页数：7

共 85 条

[11] CLONED AND EXPRESSED NITRIC-OXIDE SYNTHASE STRUCTURALLY RESEMBLES CYTOCHROME-P-450 REDUCTASE [J].

BREDT, DS ;

HWANG, PM ;

GLATT, CE ;

LOWENSTEIN, C ;

REED, RR ;

SNYDER, SH .

NATURE, 1991, 351 (6329) :714-718

[12] Synaptic signaling by nitric oxide [J].

Brenman, JE ;

Bredt, DS .

CURRENT OPINION IN NEUROBIOLOGY, 1997, 7 (03) :374-378

[13] Interaction of nitric oxide synthase with the postsynaptic density protein PSD-95 and alpha 1-syntrophin mediated by PDZ domains [J].

Brenman, JE ;

Chao, DS ;

Gee, SH ;

McGee, AW ;

Craven, SE ;

Santillano, DR ;

Wu, ZQ ;

Huang, F ;

Xia, HH ;

Peters, MF ;

Froehner, SC ;

Bredt, DS .

CELL, 1996, 84 (05) :757-767

[14] NITRIC-OXIDE SYNTHASE COMPLEXED WITH DYSTROPHIN AND ABSENT FROM SKELETAL-MUSCLE SARCOLEMMA IN DUCHENNE MUSCULAR-DYSTROPHY [J].

BRENMAN, JE ;

CHAO, DS ;

XIA, HH ;

ALDAPE, K ;

BREDT, DS .

CELL, 1995, 82 (05) :743-752

[15] Hsp90 and caveolin are key targets for the proangiogenic nitric oxide-mediated effects of statins [J].

Brouet, A ;

Sonveaux, P ;

Dessy, C ;

Moniotte, S ;

Balligand, JL ;

Feron, O .

CIRCULATION RESEARCH, 2001, 89 (10) :866-873

[16]

BUSCONI L, 1993, J BIOL CHEM, V268, P8410

[17] 3 MUSCULAR-DYSTROPHIES - LOSS OF CYTOSKELETON EXTRACELLULAR-MATRIX LINKAGE [J].

CAMPBELL, KP .

CELL, 1995, 80 (05) :675-679

[18] Involvement of presynaptic N-methyl-D-aspartate receptors in cerebellar long-term depression [J].

Casado, M ;

Isope, P ;

Ascher, P .

NEURON, 2002, 33 (01) :123-130

[19]

Chao DS, 1998, J NEUROCHEM, V71, P784

[20] Selective loss of sarcolemmal nitric oxide synthase in Becker muscular dystrophy [J].

Chao, DS ;

Gorospe, JRM ;

Brenman, JE ;

Rafael, JA ;

Peters, MF ;

Froehner, SC ;

Hoffman, EP ;

Chamberlain, JS ;

Bredt, DS .

JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 184 (02) :609-618

← 1 2 3 4 5 6 7 8 9 →