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The drug, a macrolide (polyhydroxylated lactone), is a member of a structural diverse class of compounds called polyketides with notable chemical mechanism of action. It stabilizes the microtubules of target cells, essentially arresting them at a specific stage in the cell cycle and halting cell division.
The eukaryotic cell cycle consists of four distinct phases: G 1 phase, S phase (synthesis), G 2 phase (collectively known as interphase) and M phase (mitosis and cytokinesis). M phase is itself composed of two tightly coupled processes: mitosis, in which the cell's nucleus divides, and cytokinesis, in which the cell's cytoplasm and cell membrane divides forming two daughter cells.
The cell cycle is a series of complex, ordered, sequential events that control how a single cell divides into two cells, and involves several different phases. The phases include the G1 and G2 phases, DNA replication or S phase, and the actual process of cell division, mitosis or M phase. [1]
CIP/KIP family proteins bind a wide range of G1/S and S-phase cyclin-CDK complexes including cyclin D-CDK4,6 and cyclin E-, A-CDK2 complexes. Traditionally it was assumed that CIP/KIP proteins played a role in inhibiting all of these complexes; however it was later discovered that CIP/KIP proteins, while inhibiting CDK2 activity, may also activate cyclin D-CDK4,6 activity by facilitating ...
Steps of the cell cycle. The restriction point occurs between the G 1 and S phases of interphase.. The restriction point (R), also known as the Start or G 1 /S checkpoint, is a cell cycle checkpoint in the G 1 phase of the animal cell cycle at which the cell becomes "committed" to the cell cycle, and after which extracellular signals are no longer required to stimulate proliferation. [1]
Steps of the cell cycle. The G 2-M checkpoint occurs between the G 2 and M phases. G2-M arrest. The G 2-M DNA damage checkpoint is an important cell cycle checkpoint in eukaryotic organisms that ensures that cells don't initiate mitosis until damaged or incompletely replicated DNA is sufficiently repaired.
Rather than requiring endogenous or external mitogens to continue the cell cycle, cancer cells are able to grow, survive, and replicate without mitogens. Cancer cells may lose their dependence on external mitogens by a variety of pathways. First, cancer cells can produce their own mitogens, a term called autocrine stimulation. [5]
Compared to the eukaryotic cell cycle, the prokaryotic cell cycle (known as binary fission) is relatively simple and quick: the chromosome replicates from the origin of replication, a new membrane is assembled, and the cell wall forms a septum which divides the cell into two. [7]