{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNOVA1 is an evolutionarily conserved, neuron‐specific RNA‐binding protein that functions as a master regulator of alternative splicing. In neurons, it orchestrates the processing of a wide repertoire of pre‐mRNAs required for proper synaptic activity, neuronal differentiation, and cortical development. Notably, a human‐specific amino acid substitution in NOVA1 has been shown to affect the timing of neural maturation and the complexity of synaptic networks, suggesting that fine‐tuning its splicing function may have contributed to modern human brain evolution."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a spectrum of human cancers, NOVA1 is frequently dysregulated and can exert a potent oncogenic influence. Its upregulation in astrocytomas, gastric, thyroid, hepatocellular, colorectal, melanoma, glioblastoma, head and neck, retinoblastoma, pancreatic neuroendocrine tumors, T‐cell acute lymphoblastic leukemia, and triple‐negative breast cancer has been linked to enhanced proliferation, invasion, metastasis, and even resistance to therapy. Mechanistically, NOVA1 regulates key splicing events—for example, favoring the production of full‐length hTERT mRNA to maintain telomerase activity, stabilizing mRNAs such as IL6 to potentiate downstream signaling pathways, or modulating alternative splicing events that impact the expression of oncogenic mediators. Moreover, interactions with microRNAs (e.g. miR‐181b‐5p, miR‐339, miR‐1592) or long non‐coding RNAs (e.g. MALAT1) further fine‐tune NOVA1 levels and activity in the tumor microenvironment."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its well‐established roles in neuronal development and tumor progression, NOVA1 also participates in diverse pathological and physiological processes. In the context of neurodegeneration, altered NOVA1 function and misregulated splicing contribute to early defects in diseases such as amyotrophic lateral sclerosis and C9orf72‐associated ALS, where abnormal interactions with dipeptide repeat proteins disturb cryptic exon inclusion. NOVA1 is additionally implicated in familial dysautonomia, with specific microRNAs targeting its transcripts to modulate downstream factors related to neural survival. In non‐neuronal settings, elevated NOVA1 expression in airway smooth muscle cells accentuates TGF‑β1–induced proliferation and inflammatory remodeling, and it is critically required for proper human adipogenesis through the control of endoplasmic reticulum homeostasis and chromatin accessibility."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, these studies highlight NOVA1 as a multifaceted splicing regulator whose activity not only underpins key aspects of neuronal specification and synaptic function but also drives oncogenic programs and influences cellular responses in diverse disease settings. The molecular interplay between NOVA1 and its regulatory partners—including various microRNAs, lncRNAs, and other splicing factors—offers promising avenues for the development of targeted therapies that might modulate aberrant splicing events in cancer, neurodegeneration, and metabolic disorders."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "18"}, {"type": "fg_f", "ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Antonia Ratti, Claudia Fallini, Claudia Colombrita, et al. 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