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Nitric oxide signaling: classical, less classical, and nonclassical mechanisms
Authors:Martínez-Ruiz Antonio  Cadenas Susana  Lamas Santiago
Affiliation:
  • a Servicio de Inmunología, Hospital Universitario de la Princesa, Instituto de Investigación Sanitaria Princesa (IP), Madrid, Spain
  • b Departamento de Biología Molecular, Facultad de Ciencias, Universidad Autónoma de Madrid, Madrid, Spain
  • c Centro de Biología Molecular “Severo Ochoa,” Consejo Superior de Investigaciones Científicas (CSIC), and Laboratorio Mixto CSIC-Instituto “Reina Sofía” de Investigaciones Nefrológicas, 28029 Madrid, Spain
  • Abstract:Although nitric oxide (NO) was identified more than 150 years ago and its effects were clinically tested in the form of nitroglycerine, it was not until the decades of 1970-1990 that it was described as a gaseous signal transducer. Since then, a canonical pathway linked to cyclic GMP (cGMP) as its quintessential effector has been established, but other modes of action have emerged and are now part of the common body of knowledge within the field. Classical (or canonical) signaling involves the selective activation of soluble guanylate cyclase, the generation of cGMP, and the activation of specific kinases (cGMP-dependent protein kinases) by this cyclic nucleotide. Nonclassical signaling alludes to the formation of NO-induced posttranslational modifications (PTMs), especially S-nitrosylation, S-glutathionylation, and tyrosine nitration. These PTMs are governed by specific biochemical mechanisms as well as by enzymatic systems. In addition, a less classical but equally important pathway is related to the interaction between NO and mitochondrial cytochrome c oxidase, which might have important implications for cell respiration and intermediary metabolism. Cross talk trespassing these necessarily artificial conceptual boundaries is progressively being identified and hence an integrated systems biology approach to the comprehension of NO function will probably emerge in the near future.
    Keywords:AMPK, AMP-activated protein kinase   CcO, cytochrome c oxidase   cGK, cGMP-dependent protein kinase   cGMP, cyclic GMP   EDRF, endothelial-derived relaxing factor   GAPDH, glyceraldehyde-3-phosphate dehydrogenase   GSH, reduced glutathione   GSNO, S-nitrosoglutathione   GSSG, oxidized glutathione   HIF, hypoxia-inducible factor   LMM, low molecular mass   LTP, long-term potentiation   MnSOD, manganese superoxide dismutase   mPTP, mitochondrial permeability transition pore   mtNOS, mitochondrial NOS   NO2-FA, nitro-fatty acid   NOS, nitric oxide synthase   PDE, phosphodiesterase   PFK-2, 6-phosphofructo-2-kinase   PKG, cGMP-dependent protein kinase   PTM, posttranslational modification   RNS, reactive nitrogen species   ROS, reactive oxygen species   sGC, soluble guanylate cyclase   SNO, nitrosothiol   Trx, thioredoxin
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