Journal ArticleDOI
The Bcl2 family: regulators of the cellular life-or-death switch.
Suzanne Cory,Jerry M. Adams +1 more
TLDR
A better understanding of how the Bcl2 family controls caspase activation should result in new, more effective therapeutic approaches in tissue homeostasis and cancer.Abstract:Â
Tissue homeostasis is regulated by apoptosis, the cell-suicide programme that is executed by proteases called caspases. The Bcl2 family of intracellular proteins is the central regulator of caspase activation, and its opposing factions of anti- and pro-apoptotic members arbitrate the life-or-death decision. Apoptosis is often impaired in cancer and can limit conventional therapy. A better understanding of how the Bcl2 family controls caspase activation should result in new, more effective therapeutic approaches.read more
Citations
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Journal ArticleDOI
Apoptosis: A Review of Programmed Cell Death
TL;DR: The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, the role of apoptoses in health and disease, detection methods, as well as a discussion of potential alternative forms of apoptotic proteins.
Journal ArticleDOI
miR-15 and miR-16 induce apoptosis by targeting BCL2.
Amelia Cimmino,George A. Calin,Muller Fabbri,Marilena V. Iorio,Manuela Ferracin,Masayoshi Shimizu,Sylwia E. Wojcik,Rami I. Aqeilan,Simona Zupo,Mariella Dono,Laura Z. Rassenti,Hansjuerg Alder,Stefano Volinia,Chang Gong Liu,Thomas J. Kipps,Massimo Negrini,Massimo Negrini,Carlo M. Croce +17 more
TL;DR: It is demonstrated thatmiR-15a and miR-16-1 expression is inversely correlated to Bcl2 expression in CLL and that both microRNAs negatively regulate BCL2 at a posttranscriptional level and are natural antisense B cl2 interactors that could be used for therapy of Bcl1-overexpressing tumors.
Journal ArticleDOI
Mitochondrial Membrane Permeabilization in Cell Death
TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
Journal ArticleDOI
Anticancer activities of histone deacetylase inhibitors.
TL;DR: Recent advances in the understanding of the molecular events that underlie the anticancer effects of HDAC inhibitors are summarized and how such information could be used in optimizing the development and application of these agents in the clinic, either as monotherapies or in combination with other anticancer drugs are discussed.
Journal ArticleDOI
Regulation of cell death: the calcium-apoptosis link.
TL;DR: The dual role of Ca2+ in living organisms is discussed in this paper, where it has been shown that cellular Ca 2+ overload, or perturbation of intracellular Ca2 + compartmentalization, can cause cytotoxicity and trigger either apoptotic or necrotic cell death.
References
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Journal ArticleDOI
The hallmarks of cancer.
TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
Journal ArticleDOI
Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.
TL;DR: Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.
Journal ArticleDOI
Mitochondria and apoptosis
Douglas R. Green,John C. Reed +1 more
TL;DR: A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins.
Journal ArticleDOI
Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade
Peng Li,Deepak Nijhawan,Imawati Budihardjo,Srinivasa M. Srinivasula,Manzoor Ahmad,Emad S. Alnemri,Xiaodong Wang +6 more
TL;DR: Mutation of the active site of caspase-9 attenuated the activation of cazase-3 and cellular apoptotic response in vivo, indicating that casp enzyme-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and dATP.
Journal ArticleDOI
Caspases: Enemies Within
TL;DR: This work has shown that understanding caspase regulation is intimately linked to the ability to rationally manipulate apoptosis for therapeutic gain.