{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPhospholipase C‐β1 (PLCB1) is a key enzyme in the phosphoinositide signaling cascade that hydrolyzes phosphatidylinositol 4,5‐bisphosphate (PIP2) into the second messengers inositol 1,4,5‐trisphosphate and diacylglycerol, thereby initiating calcium‐dependent and protein kinase C–mediated intracellular signaling. Its gene is organized into multiple exons with alternative splicing that gives rise to distinct isoforms with specific subcellular distributions. Notably, PLCB1 localizes not only at the plasma membrane where its activity is “tuned” by rapid substrate (PIP2) availability and by phosphorylation events that affect its interaction with regulatory proteins (for example, TRAX and α‐synuclein), but it is also enriched in the nuclear compartment where it is implicated in the regulation of cell cycle progression, cytokinesis, and gene transcription. This molecular versatility is highlighted by studies that used advanced imaging techniques to show dynamic dissociation from the membrane upon PIP2 hydrolysis and by investigations demonstrating that site‐specific phosphorylation modulates its nucleocytosolic partitioning."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its fundamental signaling role, PLCB1 has been implicated in the regulation of cell proliferation and differentiation in diverse tissues and disease contexts. In hematologic disorders, monoallelic deletions or altered expression of PLCB1 associate with myelodysplastic syndromes and evolution to acute myeloid leukemia, while in muscle cells its mis‐regulation contributes to the delayed differentiation seen in myotonic dystrophy. In the central nervous system, reduced PLCB1 levels or chromosomal deletions have been linked to neuropsychiatric disorders such as schizophrenia and, when mutated, to severe early‐onset epileptic encephalopathies. In cancer, particularly in breast cancer and cholangiocarcinoma, aberrant expression of PLCB1 promotes tumor development, metastasis, and epithelial–mesenchymal transition through activation of PI3K/AKT signaling and modulation of actin dynamics. In addition, PLCB1 participates in the regulation of cytokine production in endothelial cells and in the modulation of gene expression via interactions that counteract RNA interference. These diverse roles underscore its importance not only as a regulator of normal cell cycle and differentiation processes but also as a mediator of disease pathogenesis and as a potential prognostic marker in conditions ranging from cancer to drug‐response phenotypes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nPLCB1’s contributions to neuronal signaling and clinical outcomes are equally compelling. In neurons, nuclear pools of PLCB1 participate in the inositide cycle that may support local synthesis of endocannabinoids and modulate synaptic inputs, while in clinical settings, genetic polymorphisms and altered expression of PLCB1 have been associated with differential responses to antidepressants and susceptibility to drug dependence. Moreover, studies in glioblastoma have revealed that reduced PLCB1 expression parallels aggressive tumor phenotypes and increased invasive behavior, suggesting that maintaining proper levels of this enzyme is critical for sustaining normal cell physiology. Additional work in stem cell–derived models has identified a role for PLCB1 in osteogenic differentiation, further broadening its clinical relevance and making it an attractive target for therapeutic intervention in multiple diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "34", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Daniela Peruzzi, Michela Aluigi, Lucia Manzoli, et al. 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