nongenomic

Nongenomic refers to cellular responses to signals that do not involve changes in gene transcription. It contrasts with genomic actions, which require alterations in DNA transcription and translation. Nongenomic effects are typically rapid, occurring within seconds to minutes, whereas genomic responses often take hours to days.

These effects often arise from membrane-associated receptors or cytoplasmic signaling components. Mechanisms include activation of G protein–coupled receptors, receptor tyrosine kinases, and membrane-localized steroid hormone receptors. Triggered signaling cascades involve second messengers such as intracellular calcium, cyclic AMP, and IP3/DAG, as well as direct modulation of kinases and ion channels. Nongenomic signaling can influence vascular tone, neuronal activity, metabolism, and other rapid physiological processes.

Many hormones and neurotransmitters exhibit nongenomic actions. Estrogens, for example, can elicit rapid signaling via membrane-associated estrogen receptors and the G protein–coupled estrogen receptor GPER1, affecting cells in the brain, blood vessels, and adipose tissue. Endothelial nitric oxide synthase activation by estrogen is a classic nongenomic effect. Thyroid hormones and glucocorticoids also show non-genomic actions in certain tissues, alongside their well-known genomic effects.

Interpretation and research use: the term distinguishes quick signaling from transcriptional regulation by the same molecule. The boundary between genomic and nongenomic effects is not absolute; some responses involve both rapid signaling and later changes in gene expression.

Clinical and research relevance: understanding nongenomic signaling informs pharmacology, neuroscience, and endocrinology, with implications for drug action, tissue physiology, and the interpretation of hormonal effects.