Nitric Oxide Signaling

Nitric oxide (NO) is a short-lived free radical gas that acts as a second messenger. The 3 enzymes responsible for NO biosynthesis are endothelial, induced, and neuronal nitric oxide synthases (eNOS, iNOS, and nNOS). These enzymes have different tissue distributions, activation mechanisms, and biological functions. eNOS signaling regulates blood pressure via vascular smooth muscle contractility and blood vessel vasodilation. nNOS signaling regulates skeletal muscle contractility and central and peripheral neurotransmission, as well as synaptic signaling and plasticity. NO generated by both eNOS and nNOS signal via soluble guanylate cyclases and protein kinase G. Macrophages increase iNOS transcription to enhance their cytotoxic function in response to endotoxins and cytokines via NFκB and other intracellular signaling pathways. Increased NO levels assist in killing or slowing the growth of invading microorganisms or neoplastic tissue by inhibiting DNA synthesis and inducing double-stranded DNA breaks. NO also affects the function of endogenous and exogenous proteins by S-nitrosylation of cysteine residues. Dysregulation of these signaling pathways contributes to atherosclerosis and hypertension (eNOS), chronic inflammatory conditions and some cancers (iNOS), as well as muscular dystrophies and myopathies, stroke, and neurodegeneration (nNOS).

QIAGEN provides a broad range of assay technologies for nitric oxide signaling research that enable analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for nitric oxide signaling studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.