Kaplan, Ken - University of California, Davis - College of Biological Sciences

研究领域

Mechanisms that Govern Anaphase Progression and Mitotic Errors in Cancer We are currently engaged in two major research questions in my lab: (i) what are the pathways that ensure accurate chromosome segregation and (ii) how do perturbations in mitotic fidelity contribute to cancer? Specifically, we want to understand how the mitotic machinery responds to changes in chromosome topologies that arise during DNA replication to ensure genome integrity and how cancer cells adapt to increases in genomic instability, a process that we believe contributes to cancer cell ‘evolution’. These questions evolved from my long-standing interests in the mechanisms underlying chromosome segregation, in how defects that cause mitotic errors arise in cancer cells and in how such errors contribute to disease progression. We use budding yeast and mammalian cell culture as model systems to address mechanistic issues and mouse models for colorectal cancer to determine how mechanism contributes to disease progression. We use a wide range of experimental approaches that include genetic, biochemical and cell biology based techniques.

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Davies, A.E., Kortright, K., and Kaplan, K.B. (2015). Adenomatous polyposis coli mutants dominantly activate Hsf1-dependent cell stress pathways through inhibition of microtubule dynamics. Oncotarget. Rozelle, D.K., Hansen, S.D. & Kaplan, K.B. Chromosome passenger complexes control anaphase duration and spindle elongation via a kinesin-5 brake. J. Cell BIol. 193, 285–294 (2011). Caldwell, C. Green, R.A., Kaplan, K.B., APC mutations lead to cytokinetic failures in vitro and tetraploid genotypes in Min mice, The Journal of Cell Biology 178(7): 1109-20,2007 Thomas, S., and Kaplan, K.B. A Bir1p Sli15p kinetochore passenger complex regulates septin organization during anaphase. Mol Biol Cell. 2007; 18:3820-34. Catlett, M.G., Kaplan, K.B., Sgt1p is a unique co-chaperone that acts as a client-adaptor to link Hsp90 to Skp1p, Nov 3, 2006; 281(44):33739-48.