{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMYO1B functions as a highly adaptable molecular motor that responds to mechanical tension and drives membrane remodeling. Under low piconewton loads, MYO1B dramatically lengthens its actin attachment time, effectively acting as a tension sensor that can switch to a high duty‐ratio motor even under minimal force."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In reconstituted membrane systems, single‐headed MYO1B molecules have been shown to extract membrane tubes from lipid bilayers along bundled actin filaments, highlighting its capacity to actively remodel membranes."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": " Moreover, MYO1B coordinates actin-dependent trafficking mechanisms by regulating tubule formation at the trans-Golgi network and modulating the morphology of sorting endosomes."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAberrant regulation of MYO1B has emerged as an oncogenic event in several malignancies. In glioma, splicing factor SRSF1 facilitates the production of an oncogenic, full-length, membrane-localized MYO1B isoform that enhances tumor progression via activation of the PDK1/AKT and PAK/LIMK pathways."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " In head and neck squamous cell carcinoma (HNSCC), downregulation of specific microRNA strands leads to MYO1B overexpression and contributes to enhanced cell proliferation, migration, and invasive behavior."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": " A broader ceRNA network further implicates MYO1B in driving epithelial–mesenchymal transition and tumor spread in HNSCC"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": ", while studies in arecoline-induced oral cancer and esophageal squamous cell carcinoma reveal that MYO1B promotes malignancy by activating oncogenic signaling pathways such as the SNAI2/cyclin D1 axis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its roles in membrane dynamics and cancer progression, MYO1B has been associated with specialized cellular functions. In the sensory epithelia of the inner ear, MYO1B is differentially expressed in hair cells and supporting cells, suggesting a contributory role in mechanotransduction."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "11"}]}, {"type": "t", "text": " MYO1B also interfaces with cell-signaling pathways—it interacts with EphB2 receptors to modulate actomyosin organization and filopodia formation, thereby influencing cell repulsion."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "12"}]}, {"type": "t", "text": " Beyond this, MYO1B has been implicated in colorectal cancer, where its overexpression impairs autophagosome-lysosome fusion leading to HIF-1α accumulation and enhanced VEGF-mediated angiogenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": " Finally, its identification as a pericyte-specific marker underscores a role in vascular biology, and in endothelial cells, MYO1B disruption has been shown to restore autophagic flux, thereby alleviating cellular senescence and vascular dysfunction."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Joseph M Laakso, John H Lewis, Henry Shuman, et al. 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