Search results
Results from the WOW.Com Content Network
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]
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.
A cell that has accumulated a large amount of DNA damage or can no longer effectively repair its DNA may enter one of three possible states: an irreversible state of dormancy, known as senescence; cell suicide, also known as apoptosis or programmed cell death; unregulated cell division, which can lead to the formation of a tumor that is cancerous
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]
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]
During terminal differentiation, a precursor cell formerly capable of cell division permanently leaves the cell cycle, dismantles the cell cycle machinery and often expresses a range of genes characteristic of the cell's final function (e.g. myosin and actin for a muscle cell). Differentiation may continue to occur after terminal ...
The G1/S transition is highly regulated by transcription factor p53 in order to halt the cell cycle when DNA is damaged. [5] It is a "point of no return" beyond which the cell is committed to dividing; in yeast this is called the Start point, and in multicellular eukaryotes it is termed the restriction point (R-Point).
MCM2-7 is required for both DNA replication initiation and elongation; its regulation at each stage is a central feature of eukaryotic DNA replication. [3] During G1 phase, the two head-to-head Mcm2-7 rings serve as the scaffold for the assembly of the bidirectional replication initiation complexes at the replication origin.