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Apoptosis is a mechanism of cell death that occurs after sufficient cellular damage. It occurs normally during development and aging and is considered a vital component of cell turnover, cell development and function of the immune system. It occurs as a defense mechanism such as in immune reactions or when cells are damaged by disease or noxious agents.
Apoptosis, in general, confers advantages during an organism's life cycle. Between 50 billion and 70 billion cells die each day due to apoptosis in the average human adult. In a year, this amounts to the proliferation and subsequent destruction of a mass of cells equal to an individual's body weight. Inappropriate apoptosis is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. The ability to modulate the life or death of a cell is recognized for its profound therapeutic potential, and research continues to focus on the elucidation of the cell cycle machinery and signaling pathways that control cell cycle arrest and apoptosis.
Tocris offers the following scientific literature for Apoptosis to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.