Abstract:Apoptosis, also called programmed cell death, has attracted great attention in recent years. In 1999 there were over 9000 publications elucidating questions in the field of apoptosis. Today, we know t...Apoptosis, also called programmed cell death, has attracted great attention in recent years. In 1999 there were over 9000 publications elucidating questions in the field of apoptosis. Today, we know that apoptosis is involved in many physiological processes and that there is hardly any disease whose pathogenesis can be explained without apoptosis (either too much or too little of it). Apoptosis is characterized by membrane inversion exposure of phosphatidylserine, blebbing, chromatin condensation, DNA degradation and fragmentation of the nucleus. Apoptosis is initiated by a variety of stimuli, including growth factor withdrawal, UV or gamma irradiation, chemotherapeutic drugs and by the so-called death receptor expressed on the cell surface. During the recent years two distinct pathways leading to apoptosis have been identified. The first one is activated by oligomerization of death receptors, which recruit adapter protein to form the death inducing signaling complex involved in the activation of caspase-8. The second pathway depends on mitochondria. When the mitochondrion receives appropriate apoptotic cues, or is irreversibly damaged, pro-apoptotic molecules such as citochrome c are released in the cytosol. Together with ATP, citochrome c forms the complex, called apoptosom, with Apaf1 and procaspase 9, which is released in the active form. Initiator caspases such as caspases-8 and- 9 initiates a caspase cascade downstream of the mitochondrion, which then ultimatively leads to the execution of apoptosis.Read More
Publication Year: 2002
Publication Date: 2002-01-01
Language: en
Type: article
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Cited By Count: 6
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