Year: 2008
Type: dissertation
Abstract: The aberrant regulation of cell cycle checkpoints can potentially initiate cellular transformation to an oncogenic state that leads to tumor formation. Many families of cell cycle regulators are present to ensure that normal cellular growth and replication occurs, including the polo-like kinases (Plk). Plk4 (Sak), the newest and most structurally divergent member of the Plks has been implicated to play crucial roles in centrosome dynamics and mitotic progression. Plk4 heterozygous mouse embryonic fibroblasts (MEFs) present a number of phenotypic differences, in comparison to their wild type counterparts that may contribute to the increased incidence of tumor formation observed in heterozygous Plk4 mice. Microarray technology was employed to investigate transcriptional differences between the wild type and heterozygous Plk4 MEFs. Furthermore, transcriptional and protein differences were examined in the Plk4 MEFs in response to DNA damaging agents, to explore a possible role for Plk4 in the DNA damage pathways.
Author: Alan Morettin
Language: English
Subfield: Cell Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W141941554