{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNeogenin (NEO1) has emerged as an important co‐receptor in the regulation of bone morphogenetic protein (BMP) signaling and systemic iron homeostasis. In hepatocytes, NEO1 interacts with hemojuvelin (HJV) and related repulsive guidance molecules (RGMs) to modulate the transcription of hepcidin, a key iron regulatory hormone. Structural studies have delineated how NEO1 binds BMP2 in complex with RGMs, and in vitro studies established that while HJV–BMP signaling occurs via a defined subset of BMP ligands and receptors, the participation of NEO1 in such complexes can vary, thereby influencing HJV processing and cleavage by proteases such as matriptase‐2. Collectively, these studies indicate that NEO1 participates in—and in certain contexts modulates—the capacity of BMP signaling to affect iron metabolism."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in modulating extracellular BMP signals, NEO1 functions as a multifunctional dependence receptor that undergoes regulated proteolytic cleavage. Gamma‐secretase–mediated release of its intracellular domain (NeICD) enables NEO1 to translocate to the nucleus and influence gene transcription. In addition, through interactions with intracellular effectors such as the death‐associated protein kinase (DAPK), NEO1 can trigger pro‐apoptotic cascades in the absence of ligand engagement. Its expression in neural progenitors and mammary cap cells—as well as its regulation by morphogens like Sonic Hedgehog—support a role for NEO1 in guiding neuronal migration and cell fate decisions, with emerging links to neurodevelopmental disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "15"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn diverse cancer types, the role of NEO1 appears context dependent. In some studies, decreased NEO1 levels (for example, as mediated by microRNAs in glioblastoma or loss in glioma) correlate with enhanced tumor cell proliferation, migration, and invasion—consistent with a tumor‐suppressive function. Conversely, other investigations in gastric, ovarian, breast, hepatocellular, and melanoma models indicate that NEO1 expression can promote cell motility and survival via activation of oncogenic signaling cascades (e.g. ERK1/2, PI3K/Akt) or through modulation of epithelial–mesenchymal transition. Additionally, in neuroblastoma cells NEO1 engagement by netrin family ligands appears essential for maintaining both pro‐migratory and survival signals. These seemingly contradictory roles underscore a complex, tissue‐ and context‐specific regulation of tumorigenesis by NEO1."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNEO1 also contributes to a variety of additional biological processes that underpin tissue integrity and homeostasis. It plays a key role in maintaining epithelial adherens junction stability through the recruitment of actin regulatory complexes, thereby influencing cell–cell adhesion and cadherin recycling. In the context of pluripotent stem cells, netrin‐1 signaling via NEO1 has been shown to regulate self‐renewal and differentiation by simultaneously modulating Wnt and MAPK pathways. Furthermore, through actions in astrocytes and placental trophoblasts, NEO1 participates in the regulation of inflammatory resolution, synaptic transmission, and cell invasion during placental development."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Yin Xia, Jodie L Babitt, Yisrael Sidis, et al. 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