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Kinesin family member 14 (KIF14) is a highly conserved microtubule-dependent motor protein of the kinesin-3 superfamily. It functions in mitosis by regulating spindle formation and chromosome segregation, localizing to the spindle apparatus in early mitosis and the midbody in cytokinesis[3][4]. KIF14 has intrinsic ATPase motor activity that enables movement along microtubules. Biologically, it is essential for successful cell division, vesicle transport, and cellular proliferation, and it plays a key role in neurodevelopment and ciliary function[3][4]. Dysregulation of KIF14—typically overexpression—is implicated as a driver of oncogenic phenotypes and poor prognosis across multiple human cancers, while loss-of-function mutations are linked to developmental diseases such as primary microcephaly and Meckel syndrome[1][3][4]. KIF14 is emerging as both a potential prognostic biomarker and a possible therapeutic target in oncology and developmental pathology, though no targeted drugs are presently approved[3][4]. Its inhibition can lead to cell cycle arrest, cytokinesis failure, and apoptosis, highlighting both its clinical promise and the safety concerns of therapeutic targeting[1][3].
Induction of apoptosis and cytokinesis failure via experimental silencing or knockdown (e.g., siRNA) Increased sensitivity to chemotherapeutic agents (e.g., docetaxel) when KIF14 is suppressed Potential involvement in regulation of cell cycle via modulation of the SCF complex leading to altered degradation of cell cycle inhibitors like p27(Kip1)
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