{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTACR1, which encodes the neurokinin‑1 receptor (NK1R), is a key mediator of neuropeptide signaling in the central nervous system. Activation of NK1R by its primary ligand, substance P, regulates diverse neural processes including pain transmission, the emetic reflex, and modulation of neuronal excitability. Recent studies have detailed how NK1R displays region‐specific expression and exists in multiple isoforms, each with distinct signaling properties and cellular localizations. In particular, endosomal NK1R signaling has been implicated in sustaining nociceptive responses, while high‐resolution structural analyses have revealed unique ligand–receptor interactions that underlie its pharmacologic selectivity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its central actions, TACR1 is widely expressed in peripheral tissues and immune cells where NK1R activation modulates inflammatory responses, tissue remodeling, and cellular homeostasis. Its expression in articular cartilage, vascular smooth muscle, tendinous structures, and adenotonsillar as well as skin tissues has been linked to functions ranging from regulation of platelet aggregation and smooth muscle contractility to contributing to inflammatory skin disorders and bladder pain syndrome. In immune cells – including differentiated monocytic/macrophage populations, natural killer cells, and microglia – substance P–NK1R interactions trigger intracellular signaling cascades such as NF‑κB activation, thereby regulating cytokine production and other immunomodulatory responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "15"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDysregulated TACR1 expression and signaling have been increasingly associated with oncogenesis. In several tumor types – including pancreatic, breast, hematologic, hepatobiliary, osteosarcoma, retinoblastoma, and glioblastoma – NK1R activation promotes malignant cell proliferation, migration, angiogenesis, and resistance to apoptosis. Preclinical data further indicate that pharmacologic blockade of NK1R produces broad-spectrum antitumor effects by modulating key intracellular cascades such as those mediated by Wnt, AKT, and MAPK, and by reducing cancer stem cell markers. These findings support the development of NK1R antagonists as promising therapeutic agents in cancer management."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "26"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, emerging evidence suggests that the signaling outcomes of NK1R activation are shaped by receptor isoform diversity, post-translational modifications, and intricate interactions with intracellular adaptor proteins such as β‑arrestins. Studies employing chimeric receptor systems and high-resolution receptor crystallography have highlighted the formation of stable “signalsomes” that govern downstream ERK and MAPK activation, while genetic investigations have identified TACR1 polymorphisms correlated with neuropsychiatric conditions including attention deficit hyperactivity disorder, bipolar disorder, and alcohol dependence. Together, these insights refine our understanding of TACR1 as a multifaceted mediator of cellular signaling in both health and disease."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "30"}]}, {"type": "t", "text": ""}]}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ryo Saito, Yukio Takano, Hiro-O Kamiya "}, {"type": "b", "children": [{"type": "t", "text": "Roles of substance P and NK(1) receptor in the brainstem in the development of emesis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Pharmacol Sci (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1254/jphs.91.87"}], "href": "https://doi.org/10.1254/jphs.91.87"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12686752"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12686752"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Laura Caberlotto, Yasmin L Hurd, Paul Murdock, et al. 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