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Cells with a defective G 2-M checkpoint will undergo apoptosis or death after cell division if they enter the M phase before repairing their DNA. [1] The defining biochemical feature of this checkpoint is the activation of M-phase cyclin-CDK complexes, which phosphorylate proteins that promote spindle assembly and bring the cell to metaphase. [2]
The Novak–Tyson model is a mathematical model of cell cycle progression that predicts that irreversible transitions entering and exiting mitosis are driven by hysteresis. The model has three basic predictions that should hold true in cycling oocyte extracts whose cell cycle progression is dependent on hysteresis: [26]
Resolving the question of why cancer cells have short telomeres led to the development of a two-stage model for how cancer cells subvert telomeric regulation of the cell cycle. First, the DNA damage checkpoint must be inactivated to allow cells to continue dividing even when telomeres pass the critical length threshold.
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]
The Novak–Tyson Model is a non-linear dynamics framework developed in the context of cell-cycle control by Bela Novak and John J. Tyson. It is a prevalent theoretical model that describes a hysteretic , bistable bifurcation of which many biological systems have been shown to express.
In adults, telomerase is highly expressed only in cells that need to divide regularly, especially in male sperm cells, [29] but also in epidermal cells, [30] in activated T cell [31] and B cell [32] lymphocytes, as well as in certain adult stem cells, but in the great majority of cases somatic cells do not express telomerase. [33]
Cell-based models are mathematical models that represent biological cells as discrete entities. Within the field of computational biology they are often simply called agent-based models [1] of which they are a specific application and they are used for simulating the biomechanics of multicellular structures such as tissues. to study the influence of these behaviors on how tissues are organised ...
In order to become active, they require (potentially multiple) phosphorylation events in their activation loops. This is conducted by specialized enzymes of the STE protein kinase group. In this way protein dynamics can induce a conformational change in the structure of the protein via long-range allostery. [citation needed]