Abstract
Apoptosis is an induced and ordered process in which the cell actively participates in bringing about its own death. Dysregulation in either of the apoptotic pathways leads to various diseases including cancer, neurodegenerative disorders and autoimmunity. Bcl-2 (B cell lymphoma 2) proteins such as pro-and anti-apoptotic play a vital role in the mitochondrial pathway of apoptosis which results in cellular commitment to death or cell survival. So, therefore many small molecule antagonists that targets Bcl-2 anti-apoptotic proteins that lead to cellular survival are in their pre-clinical and clinical stages. In this review we focus on the apoptotic players of Bcl-2 group of proteins and their anti-apoptotic inhibitors.
Keywords: Apoptosis, Bcl-2 family, BH-3 Domain, Molecular pathways, Small molecule inhibitors
Current Cancer Therapy Reviews
Title:BCL-2 Family Proteins: The Mitochondrial Apoptotic Key Regulators
Volume: 8 Issue: 2
Author(s): P. Daisy and K. Saipriya
Affiliation:
Keywords: Apoptosis, Bcl-2 family, BH-3 Domain, Molecular pathways, Small molecule inhibitors
Abstract: Apoptosis is an induced and ordered process in which the cell actively participates in bringing about its own death. Dysregulation in either of the apoptotic pathways leads to various diseases including cancer, neurodegenerative disorders and autoimmunity. Bcl-2 (B cell lymphoma 2) proteins such as pro-and anti-apoptotic play a vital role in the mitochondrial pathway of apoptosis which results in cellular commitment to death or cell survival. So, therefore many small molecule antagonists that targets Bcl-2 anti-apoptotic proteins that lead to cellular survival are in their pre-clinical and clinical stages. In this review we focus on the apoptotic players of Bcl-2 group of proteins and their anti-apoptotic inhibitors.
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Cite this article as:
Daisy P. and Saipriya K., BCL-2 Family Proteins: The Mitochondrial Apoptotic Key Regulators, Current Cancer Therapy Reviews 2012; 8 (2) . https://dx.doi.org/10.2174/157339412800675414
DOI https://dx.doi.org/10.2174/157339412800675414 |
Print ISSN 1573-3947 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6301 |
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