[2] The earliest identified and best characterized IEGs include c-fos, c-myc and c-jun, genes that were found to be homologous to retroviral oncogenes.
[6] Downregulation of mRNA transcription occurs through redundant targeting of the 3' UTR region by microRNAs, resulting in translational repression and degradation.
IEGs are often the first responders to regulatory signals with many reaching peak expression within 30 minutes after stimuli compared to 2–4 hours in the case of delayed primary response gene.
[6] As such, many IEGs function as transcription factors regulating expression of downstream genes or are proto-oncogenes associated with altered cell growth.
[9] As such, IEGs are utilized as a marker to understand neuronal ensembles associated with formations of certain memories such as fear, commonly attributed to the development of psychiatric disorders.
[11] For example, neurons expression Arc in the hippocampus show phenotypic and behavioral differences in response to stimuli such as altered dendritic spine morphology or spontaneous firing rate.
[9] These findings offer insight into the molecular mechanism and functional changes brought about by IEG expression, expanding the theory of memory trace.
However, in the case of IEGs associated with memory consolidation demethylation of 5-methylcytosine to form the normal base cytosine can induce rapid gene expression.
[15] As such, IEGs are crucial markers in evaluating neuronal activity in the context of psychiatric illness with its expression pattern shaped by environmental and genetic factors.
[16] Conventional anti-viral treatments such as Ganciclovir use nucleoside analogs to target the early events of the viral replication cycles, however, these approaches are prone to developing resistance.