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Title
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Apoptosis : mechanisms and relevance in cancer
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Author
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Abstract
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| Apoptosis or programmed cell death is a process with typical morphological characteristics including plasma membrane blebbing, cell shrinkage, chromatin condensation and fragmentation. A family of cystein-dependent aspartate-directed proteases, called caspases, is responsible for the proteolytic cleavage of cellular proteins leading to the characteristic apoptotic features, e.g. cleavage of caspase-activated DNase resulting in internucleosomal DNA fragmentation. Currently, two pathways for activating caspases have been studied in detail. One starts with ligation of a death ligand to its transmembrane death receptor, followed by recruitment and activation of caspases in the death-inducing signalling complex. The second pathway involves the participation of mitochondria, which release caspase-activating proteins into the cytosol, thereby forming the apoptosome where caspases will bind and become activated. In addition, two other apoptotic pathways are emerging: endoplasmic reticulum stress-induced apoptosis and caspase-independent apoptosis. Naturally occurring cell death plays a critical role in many normal processes like foetal development and tissue homeostasis. Dysregulation of apoptosis contributes to many diseases, including cancer. On the other hand, apoptosis-regulating proteins also provide targets for drug discovery and new approaches to the treatment of cancer. |
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Language
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English
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Source (journal)
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Annals of hematology. - Berlin, 1991, currens
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Publication
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Berlin
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2005
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ISSN
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0939-5555
[print]
1432-0584
[online]
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DOI
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10.1007/S00277-005-1065-X
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Volume/pages
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84
:10
(2005)
, p. 627-639
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ISI
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000232340600001
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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