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. Author manuscript; available in PMC: 2014 May 29.
Published in final edited form as: Breast Cancer Res Treat. 2011 Apr 9;131(3):849–858. doi: 10.1007/s10549-011-1500-8

Figure 5. A point mutation in the ATP-binding domain of KIF5A inhibits KIF5A-mediated docetaxel resistance.

Figure 5

A. Empty vector (V), or retroviral constructs with KIF5A (WT), or K92R, a point mutation into the ATP-binding domain of KIF5A, were each transfected in MDA-MB-231 cells. The level of expression was determined by Western analysis, using total cell lysates. Actin protein levels as manifested by probing with a pan-actin antibody was used as a control. B. Cell survival assays were performed in cells infected with empty vector or with retroviruses encoding KIF5A, or mutant form of KIF5A (K92R), after treatment with docetaxel. The fraction of surviving cells was determined by normalizing the data from docetaxel-treated cells to untreated controls. Columns, means of three experiments: each measurement was performed in triplicate; bars, SD, **, P < 0.005.