Programmed cell death in animal development
Article Abstract:
Programmed cell death (PCD) in animal development generally refers to any cell death which is mediated by the intracellular death program, regardless of what triggers it and whether or not it exhibits the characteristics of apoptosis. Many of the PCDs that occur during the development of animals are transcriptionally controlled. PCD has five functions in animal development, namely, sculpting parts of the body, deleting unneeded structures, controlling cell numbers, eliminating abnormal, misplaced, non-functional or dangerous cells and generating differentiated cells without organelles.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
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P53, the cellular gatekeeper for growth and division
Article Abstract:
The P53 gene mediates apoptosis in cells with activated oncogenes, thus reducing the incidence of cancers. p53-mediated apoptosis slows tumor growth significantly as a T antigen mutant that cannot inactivate p53 functions in these cells is used. In senescence, p53 reacts to signals from normal cells undergoing progressive passages in culture. In late-passage cells, p53 activity and p21 levels increase, slowing or stopping the division rate of the culture. The lifespan of such cells is substantially enhanced with the addition of a transdominant-acting p53 mutant.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1997
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Size control: the regulation of cell numbers in animal development
Article Abstract:
An animal's size is determined by the number of cells it has. The higher the number, the larger the animal will be. In the case of humans, cells are more numerous because they divide more times on the average than smaller animals. However, the causes of cell division in humans, and all animals for that matter, remain unknown. Studies with mice, worms and yeasts show the need to identify cell-cycle regulators for better understanding of cell division and its mechanics.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 1996
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