ArticleProceedings of the National Academy of Sciences of the United States of America2002
Solution structure of a Bcl-2 homolog from Kaposi sarcoma virus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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53 citing papers in PubMed, 121 citations in OpenAlex.
- Kaposi's sarcoma-associated herpesvirus induces mitochondrial fission to evade host immune responses and promote viral production.Nature microbiology · 2025Article
- Review
- Molecular characterization and expression analysis of B-cell lymphoma-2 inFrontiers in immunology · 2023Article
- The Mitochondrial Pathway of Apoptosis Part II: The BCL-2 Protein Family.Cold Spring Harbor perspectives in biology · 2022Review
- Structural Insight into KsBcl-2 Mediated Apoptosis Inhibition by Kaposi Sarcoma Associated Herpes Virus.Viruses · 2022Article
- Structural Details of BH3 Motifs and BH3-Mediated Interactions: an Updated Perspective.Frontiers in molecular biosciences · 2022Review
- Designing BH3-Mimetic Peptide Inhibitors for the Viral Bcl-2 Homologues A179L and BHRF1: Importance of Long-Range Electrostatic Interactions.ACS omega · 2021Article
- Identification of AIDS-Associated Kaposi Sarcoma: A Functional Genomics Approach.Frontiers in genetics · 2019Article
- The Bcl-2 Family in Host-Virus Interactions.Viruses · 2017Review
- The N Terminus of the Vaccinia Virus Protein F1L Is an Intrinsically Unstructured Region That Is Not Involved in Apoptosis Regulation.The Journal of biological chemistry · 2016Article
- Locating Herpesvirus Bcl-2 Homologs in the Specificity Landscape of Anti-Apoptotic Bcl-2 Proteins.Journal of molecular biology · 2015Article
- Viral Bcl-2 Encoded by the Kaposi's Sarcoma-Associated Herpesvirus Is Vital for Virus Reactivation.Journal of virology · 2015Article
- Targeting γ-herpesvirus 68 Bcl-2-mediated down-regulation of autophagy.The Journal of biological chemistry · 2014Article
- Disruption of Bcl-2 and Bcl-xL by viral proteins as a possible cause of cancer.Infectious agents and cancer · 2014Review
- Structural biology of the Bcl-2 family and its mimicry by viral proteins.Cell death & disease · 2013Review
- Evolution of Bcl-2 homology motifs: homology versus homoplasy.Trends in cell biology · 2013Article
- Functions of S100 proteins.Current molecular medicine · 2013Review
- Role of the Crosstalk between Autophagy and Apoptosis in Cancer.Journal of oncology · 2013Article
- In vivo screening of S100B inhibitors for melanoma therapy.Methods in molecular biology (Clifton, N.J.) · 2013Article
- Sheeppox virus SPPV14 encodes a Bcl-2-like cell death inhibitor that counters a distinct set of mammalian proapoptotic proteins.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi sarcoma-associated herpes virus (KSHV) contains a gene that has functional and sequence homology to the apoptotic Bcl-2 family of proteins [Sarid, R., Sato, T., Bohenzky, R. A., Russo, J. J. & Chang, Y. (1997) Nat. Med. 3, 293-298]. The viral Bcl-2 protein promotes survival of infected cells and may contribute to the development of Kaposi sarcoma tumors [Boshoff, C. & Chang, Y. (2001) Annu. Rev. Med. 52, 453-470]. Here we describe the solution structure of the viral Bcl-2 homolog from KSHV. Comparison of the KSHV Bcl-2 structure to that of Bcl-2 and Bcl-x(L) shows that although the overall fold is the same, there are key differences in the lengths of the helices and loops. Binding studies on peptides derived from the Bcl-2 homology region 3 of proapoptotic family members indicate that the specificity of the viral protein is very different from what was previously observed for Bcl-x(L) and Bcl-2, suggesting that the viral protein has evolved to have a different mechanism of action than the host proteins.
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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.