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Kinesin family member 7 (KIF7) is a kinesin-4 superfamily motor protein essential for regulating microtubule dynamics and architecture, especially at the plus-ends of microtubules within the primary cilium[2][4]. KIF7 plays a pivotal role in the Hedgehog (Hh) signaling pathway by controlling the structure of the ciliary tip, thereby influencing the spatial regulation of Gli/Sufu complex activation[1][2]. In development, KIF7 is required for proper embryonic tissue patterning and organogenesis, modulating cell proliferation and differentiation by affecting the cell cycle machinery[1][3]. Mutations can lead to ciliopathies and congenital malformation syndromes (e.g., Joubert, hydrolethalus, and acrocallosal syndromes)[3]. KIF7’s absence or dysfunction results in abnormal cilia structure, aberrant Hedgehog signaling, uncontrolled cell proliferation, and potentially oncogenic transformation[1][3][4]. No specific small molecule drugs targeting KIF7 are clinically available or described in current literature.
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