ArticleThe Journal of biological chemistry2018
Grouper iridovirus GIV66 is a Bcl-2 protein that inhibits apoptosis by exclusively sequestering Bim.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Crystal structure of Bcl-2 from lymphocystis disease virus 2 in complex with the BH3 domain of zebrafish BaxA.Journal of microbiology (Seoul, Korea) · 2026Article
- Acetylation of FOXO1 activates Bim expression involved in CVB3 induced cardiomyocyte apoptosis.Apoptosis : an international journal on programmed cell death · 2024Article
- Fish Iridoviridae: infection, vaccination and immune response.Veterinary research · 2024Review
- Review
- LncGBP9 knockdown alleviates myocardial inflammation and apoptosis in mice with acute viral myocarditis via suppressing NF-κB signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Crystal Structures of Epstein-Barr Virus Bcl-2 Homolog BHRF1 Bound to Bid and Puma BH3 Motif Peptides.Viruses · 2022Article
- Article
- Structural Insight into KsBcl-2 Mediated Apoptosis Inhibition by Kaposi Sarcoma Associated Herpes Virus.Viruses · 2022Article
- Designing BH3-Mimetic Peptide Inhibitors for the Viral Bcl-2 Homologues A179L and BHRF1: Importance of Long-Range Electrostatic Interactions.ACS omega · 2021Article
- Mining prognostic markers of Asian hepatocellular carcinoma patients based on the apoptosis-related genes.BMC cancer · 2021Article
- Poxviral Strategies to Overcome Host Cell Apoptosis.Pathogens (Basel, Switzerland) · 2020Review
- Crystal structures of ORFV125 provide insight into orf virus-mediated inhibition of apoptosis.The Biochemical journal · 2020Article
- The Bcl-2 Family: Ancient Origins, Conserved Structures, and Divergent Mechanisms.Biomolecules · 2020Review
- Exosomes derived from cardiac progenitor cells attenuate CVB3-induced apoptosis via abrogating the proliferation of CVB3 and modulating the mTOR signaling pathways.Cell death & disease · 2019Article
- Viral Hormones: Expanding Dimensions in Endocrinology.Endocrinology · 2019Review
- Crystal Structure of African Swine Fever Virus A179L with the Autophagy Regulator Beclin.Viruses · 2019Article
- A new crystal structure and small-angle X-ray scattering analysis of the homodimer of human SFPQ.Acta crystallographica. Section F, Structural biology communications · 2019Article
- A structural investigation of NRZ mediated apoptosis regulation in zebrafish.Cell death & disease · 2018Article
- Human β-defensin 2 killsScience advances · 2018Article
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
Programmed cell death or apoptosis is a critical mechanism for the controlled removal of damaged or infected cells, and proteins of the Bcl-2 family are important arbiters of this process. Viruses have been shown to encode functional and structural homologs of Bcl-2 to counter premature host-cell apoptosis and ensure viral proliferation or survival. Grouper iridovirus (GIV) is a large DNA virus belonging to the Iridoviridae family and harbors GIV66, a putative Bcl-2-like protein and mitochondrially localized apoptosis inhibitor. However, the molecular and structural basis of GIV66-mediated apoptosis inhibition is currently not understood. To gain insight into GIV66's mechanism of action, we systematically evaluated its ability to bind peptides spanning the BH3 domain of pro-apoptotic Bcl-2 family members. Our results revealed that GIV66 harbors an unusually high level of specificity for pro-apoptotic Bcl-2 and displays affinity only for Bcl-2-like 11 (Bcl2L11 or Bim). Using crystal structures of both apo-GIV66 and GIV66 bound to the BH3 domain from Bim, we unexpectedly found that GIV66 forms dimers via an interface that results in occluded access to the canonical Bcl-2 ligand-binding groove, which breaks apart upon Bim binding. This observation suggests that GIV66 dimerization may affect GIV66's ability to bind host pro-death Bcl-2 proteins and enables highly targeted virus-directed suppression of host apoptosis signaling. Our findings provide a mechanistic understanding for the potent anti-apoptotic activity of GIV66 by identifying it as the first single-specificity, pro-survival Bcl-2 protein and identifying a pivotal role of Bim in GIV-mediated inhibition of apoptosis.
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