ArticleJournal of virology2000
Antiapoptotic herpesvirus Bcl-2 homologs escape caspase-mediated conversion to proapoptotic proteins.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
50 citing papers in PubMed, 132 citations in OpenAlex.
- Bcl-xL is required to protect endothelial cells latently infected with KSHV from virus induced intrinsic apoptosis.PLoS pathogens · 2023Article
- Kaposi Sarcoma, a Trifecta of Pathogenic Mechanisms.Diagnostics (Basel, Switzerland) · 2022Review
- Structural Insight into KsBcl-2 Mediated Apoptosis Inhibition by Kaposi Sarcoma Associated Herpes Virus.Viruses · 2022Article
- Viral Bcl2s' transmembrane domain interact with host Bcl2 proteins to control cellular apoptosis.Nature communications · 2020Article
- Transient Unfolding and Long-Range Interactions in Viral BCL2 M11 Enable Binding to the BECN1 BH3 Domain.Biomolecules · 2020Article
- Mitochondrial Degeneration and Autophagy Associated With Delayed Effects of Radiation in the Mouse Brain.Frontiers in aging neuroscience · 2019Article
- The Viral Bcl-2 Homologs of Kaposi's Sarcoma-Associated Herpesvirus and Rhesus Rhadinovirus Share an Essential Role for Viral Replication.Journal of virology · 2017Article
- Viral Bcl-2 Encoded by the Kaposi's Sarcoma-Associated Herpesvirus Is Vital for Virus Reactivation.Journal of virology · 2015Article
- A gammaherpesvirus Bcl-2 ortholog blocks B cell receptor-mediated apoptosis and promotes the survival of developing B cells in vivo.PLoS pathogens · 2014Article
- Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer.Infectious agents and cancer · 2014Review
- Article
- Engineering lentiviral vectors for modulation of dendritic cell apoptotic pathways.Virology journal · 2013Article
- Evasion of adaptive and innate immune response mechanisms by γ-herpesviruses.Current opinion in virology · 2013Review
- Multiple functions of BCL-2 family proteins.Cold Spring Harbor perspectives in biology · 2013Review
- The Role of BCL2 Family of Apoptosis Regulator Proteins in Acute and Chronic Leukemias.Advances in hematology · 2012Article
- TLR9-induced interferon β is associated with protection from gammaherpesvirus-induced exacerbation of lung fibrosis.Fibrogenesis & tissue repair · 2011Article
- Immune evasion by Kaposi's sarcoma-associated herpesvirus.Future microbiology · 2010Review
- GLTSCR2/PICT-1, a putative tumor suppressor gene product, induces the nucleolar targeting of the Kaposi's sarcoma-associated herpesvirus KS-Bcl-2 protein.Journal of virology · 2010Article
- Viral Bcl-2-mediated evasion of autophagy aids chronic infection of gammaherpesvirus 68.PLoS pathogens · 2009Article
- Human tumor-associated viruses and new insights into the molecular mechanisms of cancer.Oncogene · 2008Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The antiapoptotic Bcl-2 and Bcl-x(L) proteins of mammals are converted into potent proapoptotic factors when they are cleaved by caspases, a family of apoptosis-inducing proteases (E. H.-Y. Cheng, D. G. Kirsch, R. J. Clem, R. Ravi, M. B. Kastan, A. Bedi, K. Ueno, and J. M. Hardwick, Science 278:1966-1968, 1997; R. J. Clem, E. H.-Y. Cheng, C. L. Karp, D. G. Kirsch, K. Ueno, A. Takahashi, M. B. Kastan, D. E. Griffin, W. C. Earnshaw, M. A. Veliuona, and J. M. Hardwick, Proc. Natl. Acad. Sci. USA 95:554-559, 1998). Gamma herpesviruses also encode homologs of the Bcl-2 family. All tested herpesvirus Bcl-2 homologs possess antiapoptotic activity, including the more distantly related homologs encoded by murine gammaherpesvirus 68 (gammaHV68) and bovine herpesvirus 4 (BHV4), as described here. To determine if viral Bcl-2 proteins can be converted into death factors, similar to their cellular counterparts, five herpesvirus Bcl-2 homologs from five different viruses were tested for their susceptibility to caspases. Only the viral Bcl-2 protein encoded by gammaHV68 was susceptible to caspase digestion. However, unlike the caspase cleavage products of cellular Bcl-2, Bcl-x(L), and Bid, which are potent inducers of apoptosis, the cleavage product of gammaHV68 Bcl-2 lacked proapoptotic activity. KSBcl-2, encoded by the Kaposi's sarcoma-associated herpesvirus, was the only viral Bcl-2 homolog that was capable of killing cells when expressed as an N-terminal truncation. However, because KSBcl-2 was not cleavable by caspases, the latent proapoptotic activity of KSBcl-2 apparently cannot be released. The Bcl-2 homologs encoded by herpesvirus saimiri, Epstein-Barr virus, and BHV4 were not cleaved by apoptotic cell extracts and did not possess latent proapoptotic activities. Thus, herpesvirus Bcl-2 homologs escape negative regulation by retaining their antiapoptotic activities and/or failing to be converted into proapoptotic proteins by caspases during programmed cell death.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.