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In some experiments, a researcher may want to control and synchronize the time when a group of cells progress to the next phase of the cell cycle. [5] The cells can be induced to arrest as they arrive (at different time points) at a certain phase, so that when the arrest is lifted (for instance, rescuing cell cycle progression by introducing another chemical) all the cells resume cell cycle ...
Aphidicolin is a reversible inhibitor of eukaryotic nuclear DNA replication. It blocks the cell cycle at early S phase . It is a specific inhibitor of DNA polymerase Alpha and Delta in eukaryotic cells and in some viruses ( vaccinia [ 1 ] [ 2 ] and herpesviruses ) and an apoptosis inducer in HeLa cells.
The cell cycle checkpoints play an important role in the control system by sensing defects that occur during essential processes such as DNA replication or chromosome segregation, and inducing a cell cycle arrest in response until the defects are repaired. [8]
"7+3" in the context of chemotherapy is an acronym for a chemotherapy regimen that is most often used today (as of 2014) as first-line induction therapy (to induce remission) in acute myelogenous leukemia, [1] [2] excluding the acute promyelocytic leukemia form, which is better treated with ATRA and/or arsenic trioxide and requires less chemotherapy (if requires it at all, which is not always ...
APC activity also causes the destruction of S and M cyclins and thus the inactivation of Cdks, which promotes the completion of mitosis and cytokinesis. APC activity is maintained in G1 until G1/S–Cdk activity rises again and commits the cell to the next cycle. This scheme serves only as a general guide and does not apply to all cell types. [1]
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.
This delay between cell-cell contact and onset of proliferation inhibition is shortened as the culture becomes more confluent. Thus, it may be reasonably concluded that cell-cell contact is an essential condition for contact inhibition of proliferation, but is by itself insufficient for mitotic inhibition.
The enlarged cells that are able to re-enter the cell cycle are prone to DNA damage and experience abnormalities in signaling for repair (NHEJ pathway), eventually leading to a replication failure and a permanent cell-cycle exit. [24] Overall, a consistent correlation between larger cell size and senescence has been established.