6533b7dbfe1ef96bd126ffd0

RESEARCH PRODUCT

Expressional control of the ‘constitutive’ isoforms of nitric oxide synthase (NOS I and NOS III)

Hartmut KleinertJean-paul BoisselUlrich Förstermann

subject

LipopolysaccharidesGene isoformNitric Oxide Synthase Type IIITranscription GeneticNOS1Nitric Oxide Synthase Type IBiochemistryTranscription (biology)GeneticsTranscriptional regulationAnimalsHumansRNA MessengerGrowth SubstancesMolecular BiologyTranscription factorRegulation of gene expressionPolymorphism GeneticbiologyChemistryChromosome MappingLysophosphatidylcholinesNitric Oxide Synthase Type IIIEstrogensExonsCell biologyIsoenzymesLipoproteins LDLOxygenNitric oxide synthaseGene Expression Regulationbiology.proteinCytokinesNitric Oxide SynthaseGene DeletionBiotechnology

description

Nitric oxide synthase (NOS) exists in three established isoforms. NOS I (NOS1, ncNOS) was originally discovered in neurons. This enzyme and splice variants thereof have since been found in many other cells and tissues. NOS II (NOS2, iNOS) was first identified in murine macrophages, but can also be induced in many other cell types. NOS III (NOS3, ecNOS) is expressed mainly in endothelial cells. Whereas NOS II is a transcriptionally regulated enzyme, NOS I and NOS III are considered constitutively expressed proteins. However, evidence generated in recent years indicates that these two isoforms are also subject to expressional regulation. In view of the important biological functions of these isoforms, changes in their expression may have physiological and pathophysiological consequences. This review recapitulates compounds and conditions that modulate the expression of NOS I and NOS III, summarizes transcriptional and posttranscriptional effects that underlie these changes, and-where known-describes the molecular mechanisms leading to changes in transcription, RNA stability, or translation of these enzymes.

https://doi.org/10.1096/fasebj.12.10.773