NITRIC-OXIDE - A SIGNAL FOR ADP-RIBOSYLATION OF PROTEINS

被引:115
作者
BRUNE, B [1 ]
DIMMELER, S [1 ]
VEDIA, LMY [1 ]
LAPETINA, EG [1 ]
机构
[1] BURROUGHS WELLCOME CO,DIV CELL BIOL,RES TRIANGLE PK,NC 27709
关键词
D O I
10.1016/0024-3205(94)00775-6
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Nitric oxide (NO), a highly reactive gas, is now established as a major messenger molecule regulating blood vessel dilation. immune functions and serving as a neurotransmitter in brain and peripheral nervous system. NO can also act as a tumoricidal and bactericidal molecule. The effect of NO to dilate blood vessels is largely explained by stimulation of soluble guanylate cyclase (a heme-iron containing protein) leading to formation of cGMP and protein phosphorylation. This is considered to be the main physiological signaling mechanism of NO. NO also binds to non-heme iron-containing-proteins and this has been considered as a pathophysiological or cytotoxic action of NO. Furthermore, NO, more correctly nitrosonium (NO+) which can be formed by the removal of one electron, reacts with protein SH-groups to cause the S-nitrosylation of proteins. We have recently established a link between NO and the S-nitrosylation and mono-ADP-ribosylation of the enzyme glyceraldehyde 3-mopophosphate dehydrogenase, which adds a further protein modification mechanism for NO action. This links the formation of the second messenger molecule NO to post-translational protein modification and adds a new dimension to NO in the communication of intracellular signals.
引用
收藏
页码:61 / 70
页数:10
相关论文
共 55 条
[1]  
ALTHAUS FR, 1987, ADP RIBOSYLATION PRO
[2]   NITRIC-OXIDE ACTIVATES GUANYLATE CYCLASE AND INCREASES GUANOSINE 3'-5'-CYCLIC MONOPHOSPHATE LEVELS IN VARIOUS TISSUE PREPARATIONS [J].
ARNOLD, WP ;
MITTAL, CK ;
KATSUKI, S ;
MURAD, F .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1977, 74 (08) :3203-3207
[3]   INDUCIBLE CYTOSOLIC ENZYME-ACTIVITY FOR THE PRODUCTION OF NITROGEN-OXIDES FROM L-ARGININE IN HEPATOCYTES [J].
BILLIAR, TR ;
CURRAN, RD ;
STUEHR, DJ ;
STADLER, J ;
SIMMONS, RL ;
MURRAY, SA .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 168 (03) :1034-1040
[4]   NITRIC-OXIDE, A NOVEL NEURONAL MESSENGER [J].
BREDT, DS ;
SNYDER, SH .
NEURON, 1992, 8 (01) :3-11
[5]   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
[6]  
BRUNE B, 1989, J BIOL CHEM, V264, P8455
[7]   NADPH - A STIMULATORY COFACTOR FOR NITRIC OXIDE-INDUCED ADP-RIBOSYLATION REACTION [J].
BRUNE, B ;
DIMMELER, S ;
LAPETINA, EG .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1992, 182 (03) :1166-1171
[8]   PROPERTIES OF A NOVEL NITRIC OXIDE-STIMULATED ADP-RIBOSYLTRANSFERASE [J].
BRUNE, B ;
LAPETINA, EG .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1990, 279 (02) :286-290
[9]   DOES NITRIC-OXIDE MEDIATE AUTOIMMUNE DESTRUCTION OF BETA-CELLS - POSSIBLE THERAPEUTIC INTERVENTIONS IN IDDM [J].
CORBETT, JA ;
MCDANIEL, ML .
DIABETES, 1992, 41 (08) :897-903
[10]   NITRIC-OXIDE MEDIATES GLUTAMATE NEUROTOXICITY IN PRIMARY CORTICAL CULTURES [J].
DAWSON, VL ;
DAWSON, TM ;
LONDON, ED ;
BREDT, DS ;
SNYDER, SH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (14) :6368-6371