| From sentencing to execution--the processes of apoptosis. | |
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MedLine Citation:
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PMID: 20609056 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVES: Cell proliferation and apoptosis play a major role in maintaining homeostasis and as such any disruption within these processes can lead to disease states. Apoptosis occurs in three non-distinct phases--induction, effector and degradation--and can be executed through both the extrinsic and intrinsic pathways in addition to recognised sub-pathways such as the p53 and lysosomal pathways. This review article highlights these pathways, incorporating an overview of the molecular regulators of apoptosis. KEY FINDINGS: These regulators include the prominent apoptotic players 'the caspases' in addition to the main regulators of the Bcl-2 family. Increased understanding of the physiological processes of apoptosis at the molecular level not only offers an insight in disease pathogenesis but, in addition, allows for the development of diagnostic, prognostic and therapeutic tools. SUMMARY: While apoptosis remains the key player in cellular death, other processes cannot be dismissed. Many other proteins, in addition to caspases, within apoptotic pathways have been identified. Research continues into establishing the precise aspects of their molecular mechanisms of action and inter-relationships. Inappropriate apoptosis due to dysregulation of cell death pathways provides a plethora of molecular checkpoints that can be targeted and modulated as part of therapeutic intervention. Increased research into these areas will prove useful for the design of novel chemotherapeutic drugs, an area that is particularly important due to increased risk of chemoresistance. |
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Authors:
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Kelly L Moffitt; S Lorraine Martin; Brian Walker |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: The Journal of pharmacy and pharmacology Volume: 62 ISSN: 2042-7158 ISO Abbreviation: J. Pharm. Pharmacol. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-07-08 Completed Date: 2011-01-31 Revised Date: 2011-09-13 |
Medline Journal Info:
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Nlm Unique ID: 0376363 Medline TA: J Pharm Pharmacol Country: England |
Other Details:
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Languages: eng Pagination: 547-62 Citation Subset: IM |
Affiliation:
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Biomolecular Sciences Group, School of Pharmacy, Queen's University of Belfast, Belfast, Northern Ireland, UK. k.moffitt@qub.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis
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physiology* Caspases / metabolism Cell Proliferation Homeostasis Humans Mitochondria / physiology* Proteins / metabolism Proto-Oncogene Proteins c-bcl-2 / metabolism Signal Transduction |
| Chemical | |
Reg. No./Substance:
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0/Proteins; 0/Proto-Oncogene Proteins c-bcl-2; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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