Validating aurora b as an anticancer drug target Free send and receive sex sites

We exploited a hypermutagenic cancer cell line to select mutations conferring resistance to a well-studied Aurora inhibitor, ZM447439.

Fortunately, the emergence of high-throughput techniques, such as short hairpin RNA (sh RNA) screening [], has led to substantial advances in our understanding of human cancer biology.While the wealth of information in these datasets presents an opportunity to leverage these for finding novel drug targets, it remains a challenge to systematically integrate all these highly heterogeneous sources of information to identify novel anti-cancer drug targets.The Aurora kinases are a family of highly conserved serine/threonine kinases that are important for faithful transition through mitosis (1–3).The gene for Aurora-A, maps to chromosome region 20q13.2, a region that has been found amplified in different human cancers.In this review, current antimitotic agents are summarized with particular emphasis on the evaluation of their clinical efficacy as well as their limitations.

In addition, we discuss the basis behind the lack of activity of these inhibitors in human trials and the potential and future directions of mitotic anticancer strategies.The reconstitution calculator allows you to quickly calculate the volume of a reagent to reconstitute your vial.Simply enter the mass of reagent and the target concentration and the calculator will determine the rest.Aurora-A plays an important role in centrosome maturation, spindle assembly, meiotic maturation, and metaphase I spindle orientation [Figure 1 (2)].Aurora-A function is regulated by degradation, phosphorylation, and dephosphorylation, with its kinase activity dependent upon phosphorylation of threonine 288 (Thr288) in the activation loop (2).Mitosis is an elaborate process in actively proliferating cells, resulting in the division of duplicated sets of chromosomes and two genetically identical daughter cells.