{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNPAS2 encodes a basic helix–loop–helix PAS domain transcription factor that is indispensable for the maintenance of the mammalian circadian clock. In cooperation with its partner BMAL1, NPAS2 drives the rhythmic transcription of essential clock‐controlled genes and is itself subjected to tight regulation by posttranslational modifications and nuclear receptors (e.g., RORα and REV-ERBα). This dynamic regulation ensures the proper oscillation of clock gene expression and synchronizes physiological processes with day–night cycles."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic variations in NPAS2 have been robustly linked to mood and sleep disorders. Several case–control studies report associations of NPAS2 polymorphisms with major mood disorders, seasonal affective disorder, diurnal preference, and even aspects of neurodevelopmental conditions such as autism. These findings cumulatively suggest that alterations in NPAS2 can disrupt circadian phase and amplitude, thereby contributing to depression, bipolarity, and abnormal sleep–wake patterns."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its central role in circadian timing, NPAS2 is increasingly recognized as a key player in tumorigenesis and metabolic regulation. A series of genetic association studies and functional analyses have implicated NPAS2 variants in altered risk and patient outcomes in diverse cancers—including breast, non‐Hodgkin’s lymphoma, colorectal, hepatocellular, prostate, lung, and melanoma—likely through its effects on cell cycle regulation, DNA damage repair, and metabolic reprogramming (e.g., via modulation of CDC25A expression and glucose metabolism). In essence, NPAS2 exerts tumor suppressor–like functions, and its differential expression or mutation can serve as a biomarker for tumor aggressiveness and prognosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional lines of evidence indicate that NPAS2 dysregulation may also impact other disease states. Altered methylation patterns of the NPAS2 promoter have been observed in early Parkinson’s disease, while functional polymorphisms in NPAS2 are linked to susceptibility in chronic lymphocytic leukemia. Moreover, NPAS2 has been implicated in the metabolic disturbances observed in obstructive sleep apnea, which in turn may predispose individuals to type 2 diabetes. These findings broaden the biological significance of NPAS2 beyond its classical role in circadian regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "33", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Roman V Kondratov, Anna A Kondratova, Choogon Lee, et al. 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