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Kinesin family member 26B (KIF26B) is a large, evolutionarily conserved protein of the kinesin superfamily, specifically classified within the Kinesin-11 family[2][4][7]. Unlike conventional kinesins, KIF26B associates with microtubules but lacks canonical ATP-dependent motility[2]. It plays a critical role in embryonic development, including kidney morphogenesis, neural development, and endothelial cell polarity[1][2][4][8]. KIF26B is regulated by the Wnt5a-Ror noncanonical signaling pathway, which modulates its cellular stability via ubiquitin-proteasome-mediated degradation[7]. It influences cell migration, adhesion, and polarity, often localizing to the trailing edge of migrating cells[4][7]. Dysregulation or mutation of KIF26B is associated with various congenital abnormalities and is emerging as an independent prognostic biomarker and potential therapeutic target in several cancers, although there are currently no specific targeted therapeutics approved[5]. The protein's essential function in organogenesis raises safety concerns regarding potential developmental toxicity if directly inhibited.
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