Conversion of lytic to persistent alphavirus infection by the bcl-2 cellular oncogene
Article Abstract:
Sindbis virus (SV) is a member of the alphavirus genus which causes lytic infection in most vertebrate cells. However, in some post-mitotic neurons apoptosis is blocked by the function of the cellular oncogene bcl-2. Baby hamster kidney, mouse neuroblastoma and rat prostatic adenocarcinoma cells infected with SV underwent apoptosis while similar cells transfected with the bcl-2 gene had a long-term persistent productive infection. Expression of the cellular blc-2 oncogene blocks SV-induced cell death resulting in a persistent infection.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1993
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Bcl-2 blocks apoptosis in cells lacking mitochondrial DNA
Article Abstract:
Research concerning the membrane-related protein Bcl-2 demonstrated that apoptosis can affect cells lacking in mitochondrial DNA due to removal of survival factors or excessive levels of staurosporine. However, apoptosis can be prevented by overexpressing the proto-oncogene bcl-2. This overexpression has little impact on respiratory chain activity. The Bcl-2 protein is also linked to the endoplasmic reticulum and the cellular nuclear envelope.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1993
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Humanin peptide suppresses apoptosis by interfering with bax activation
Article Abstract:
Research shows that the apoptosis-inducing Bcl2-associated X protein (Bax) interacts with the the anti-apoptotic humanin peptide of mammalian genomes and prevens Bax translocation from cytosol to mitochondria. However, Bax activation and its translocation to mitochondrial membrane is a prerequisite for its apoptotic activity by releasing cytochrome c and other apoptogenic proteins.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 2003
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