| VDAC blockage by phosphorothioate oligonucleotides and its implication in apoptosis. | |
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MedLine Citation:
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PMID: 22236836 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Apoptosis is a crucial process that regulates the homeostasis of multicellular organisms. Impaired apoptosis contributes to cancer development, while enhanced apoptosis is detrimental in neurodegenerative diseases. The intrinsic apoptotic pathway is initiated by cytochrome c release from mitochondria. Research published in the recent decade has suggested that cytochrome c release can be influenced by the conducting states of VDAC, the channel in the mitochondrial outer membrane (MOM) responsible for metabolite flux. This review will describe the evidence that VDAC gating or blockage and subsequent changes in MOM permeability influence cytochrome c release and the onset of apoptosis. The blockage of VDAC by G3139, a proapoptotic phosphorothioate oligonucleotide, provides strong evidence for the role of VDAC in the initiation of apoptosis. The proapoptotic activity and VDAC blockage are linked in that both require the PS (phosphorothioate) modification, both are enhanced by an increase in oligonucleotide length, and both are insensitive to the nucleotide sequence. Thus, the mitochondrial outer membrane permeability regulated by VDAC gating may play an important role in mitochondrial function and in the control of apoptosis. This article is part of a Special Issue entitled: VDAC structure, function, and regulation of mitochondrial metabolism. |
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Authors:
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Wenzhi Tan |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-1-4 |
Journal Detail:
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Title: Biochimica et biophysica acta Volume: - ISSN: 0006-3002 ISO Abbreviation: - Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2012-1-12 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0217513 Medline TA: Biochim Biophys Acta Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012. Published by Elsevier B.V. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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