ArticleThe Journal of experimental medicine2000
M11L: a novel mitochondria-localized protein of myxoma virus that blocks apoptosis of infected leukocytes.
Article in The Journal of experimental medicine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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
64 citing papers in PubMed, 130 citations in OpenAlex.
- African swine fever virus pE199L, as a mitophagy receptor, suppresses antiviral innate immunity to promote viral replication.Autophagy · 2026Article
- Lumpy Skin Disease Virus Pathogenesis: Viral Protein Functions and Comparative Insights from Vaccinia Virus.Animals : an open access journal from MDPI · 2025Review
- The Role of Myxoma Virus Immune Modulators and Host Range Factors in Pathogenesis and Species Leaping.Viruses · 2025Review
- Cross-species transmission and host range genes in poxviruses.Virologica Sinica · 2024Review
- Granzymes in health and diseases: the good, the bad and the ugly.Frontiers in immunology · 2024Review
- Navigating the human-monkeypox virus interactome: HuPoxNET atlas reveals functional insights.Frontiers in microbiology · 2024Article
- Article
- The Bcl-2 Family: Ancient Origins, Conserved Structures, and Divergent Mechanisms.Biomolecules · 2020Review
- Oncolytic Virotherapy with Myxoma Virus.Journal of clinical medicine · 2020Review
- Coxsackievirus B infection induces the extracellular release of miR-590-5p, a proviral microRNA.Virology · 2019Article
- Article
- Caspase-Dependent Apoptosis Induction via Viral Protein ORF4 of Porcine Circovirus 2 Binding to Mitochondrial Adenine Nucleotide Translocase 3.Journal of virology · 2018Article
- Mitochondria-associated membranes (MAMs) and inflammation.Cell death & disease · 2018Review
- Orf Virus Encoded Protein ORFV119 Induces Cell Apoptosis Through the Extrinsic and Intrinsic Pathways.Frontiers in microbiology · 2018Article
- The Bcl-2 Family in Host-Virus Interactions.Viruses · 2017Review
- Review
- M011L-deficient oncolytic myxoma virus induces apoptosis in brain tumor-initiating cells and enhances survival in a novel immunocompetent mouse model of glioblastoma.Neuro-oncology · 2016Article
- Effect of bovine adenovirus 3 on mitochondria.Veterinary research · 2014Article
- Poxviruses and the evolution of host range and virulence.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2014Review
- Oncolytic Immunotherapy: Dying the Right Way is a Key to Eliciting Potent Antitumor Immunity.Frontiers in oncology · 2014Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
M11L, a novel 166-amino acid membrane-associated protein expressed by the poxvirus, myxoma virus, was previously found to modulate apoptosis after infection of rabbit leukocytes. Furthermore, infection of rabbits with an M11L knockout virus unexpectedly produced lesions with a profound proinflammatory phenotype. We show here that M11L is antiapoptotic when expressed independently of other viral proteins, and is directed specifically to mitochondria by a short COOH-terminal region that is necessary and sufficient for targeting. This targeting region consists of a hydrophobic domain flanked by basic amino acid residues, adjacent to a positively charged tail. M11L blocks staurosporine-induced apoptosis by preventing mitochondria from undergoing a permeability transition, and the mitochondrial localization of this protein is essential for this function. We show that M11L is specifically required to inhibit the apoptotic response of monocytes/macrophages during virus infection, as cells of this lineage undergo apoptosis when infected with the M11L knockout virus. As monocyte apoptosis is uniquely proinflammatory, we propose that this observation reconciles the paradoxical proapoptotic and proinflammatory phenotypes of the M11L knockout virus. We suggest that apoptosis of tissue macrophages represents an important antiviral defense, and that the inhibition of apoptosis by viral proteins can be directed in a cell-specific fashion.
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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.