The depletion of KIF18A showed a trend toward increased cyclin B1 (G2M marker) and cl-PARP (apoptosis marker) protein levels as well as decreased MCL-1 (a pro-survival marker) protein levels in those cancer cell lines sensitive to KIF18A KD in our cell growth assay (Fig. 1e ).
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Small-molecule inhibition of kinesin KIF18A reveals a mitotic vulnerability enriched in chromosomally unstable cancers.
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