Abstract
Herpesviruses, including human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), and Kaposi's sarcoma-associated herpesvirus, establish latency by modulating or mimicking antiapoptotic Bcl-2 proteins to promote survival of carrier cells. BH3 profiling, which assesses the contribution of Bcl-2 proteins towards cellular survival, was able to globally determine the level of dependence on individual cellular and viral Bcl-2 proteins within latently infected cells. Moreover, BH3 profiling predicted the sensitivity of infected cells to small-molecule inhibitors of Bcl-2 proteins.
Copyright © 2015, American Society for Microbiology. All Rights Reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Apoptosis
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Cell Line
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Cell Survival
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Cytomegalovirus / pathogenicity
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Cytomegalovirus / physiology
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Herpesviridae / pathogenicity*
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Herpesviridae / physiology*
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Herpesviridae Infections / metabolism
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Herpesviridae Infections / pathology
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Herpesviridae Infections / virology
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Herpesvirus 4, Human / pathogenicity
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Herpesvirus 4, Human / physiology
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Herpesvirus 8, Human / pathogenicity
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Herpesvirus 8, Human / physiology
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Host-Pathogen Interactions
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Humans
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Molecular Sequence Data
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Protein Array Analysis
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism*
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Viral Proteins / metabolism
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Virus Latency
Substances
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Proto-Oncogene Proteins c-bcl-2
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Viral Proteins