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Neurogenic gene expression refers to the coordinated activation of a specific set of genes required for the commitment, differentiation, and maturation of neural stem cells into functional neurons [2, 11]. This biological process is governed by a complex interplay of proneural transcription factors, such as the Neurogenin family (NEUROG1, NEUROG2) and ASCL1, which are often controlled by the Notch signaling pathway and epigenetic modifiers like histone deacetylases (HDACs) and the demethylase JMJD3 [3, 11, 14]. In the context of therapeutic development, modulating neurogenic gene expression is a strategy aimed at promoting brain repair following injury or neurodegeneration, as well as inhibiting the "hijacking" of these programs by certain cancers like glioblastoma [1, 16]. Drugs such as valproic acid and retinoic acid are known to induce this program by altering the epigenetic landscape or activating specific nuclear receptors [2, 11]. While not a single molecular target, the "neurogenic program" is a focal point for drugs that aim to enhance endogenous neurogenesis or direct cell fate in regenerative medicine [17]. Because it represents a broad transcriptional state rather than a single protein, "Neurogenic gene expression" is considered a phenotypic or pathway-level target rather than a discrete molecular receptor or enzyme [1, 13].
Induction of proneural transcription factors and epigenetic remodeling (e.g., HDAC inhibition) to promote neuronal fate commitment and differentiation.
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