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      Viral FLICE-inhibitory proteins (FLIPs) prevent apoptosis induced by death receptors.


      Adaptor Proteins, Signal Transducing, Amino Acid Sequence, Animals, Antigens, CD95, metabolism, Apoptosis, Apoptosis Regulatory Proteins, Carrier Proteins, Caspase 8, Caspase 9, Caspases, Cell Line, Cell Transformation, Viral, Cysteine Endopeptidases, Fas-Associated Death Domain Protein, Gammaherpesvirinae, genetics, physiology, Herpesvirus 2, Saimiriine, Humans, Membrane Glycoproteins, Mice, Molecular Sequence Data, Receptors, Tumor Necrosis Factor, Receptors, Tumor Necrosis Factor, Member 25, Sequence Homology, Amino Acid, Signal Transduction, TNF-Related Apoptosis-Inducing Ligand, Tumor Necrosis Factor-alpha, Viral Proteins, Virus Replication

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          Viruses have evolved many distinct strategies to avoid the host's apoptotic response. Here we describe a new family of viral inhibitors (v-FLIPs) which interfere with apoptosis signalled through death receptors and which are present in several gamma-herpesviruses (including Kaposi's-sarcoma-associated human herpesvirus-8), as well as in the tumorigenic human molluscipoxvirus. v-FLIPs contain two death-effector domains which interact with the adaptor protein FADD, and this inhibits the recruitment and activation of the protease FLICE by the CD95 death receptor. Cells expressing v-FLIPs are protected against apoptosis induced by CD95 or by the related death receptors TRAMP and TRAIL-R. The herpesvirus saimiri FLIP is detected late during the lytic viral replication cycle, at a time when host cells are partially protected from CD95-ligand-mediated apoptosis. Protection of virus-infected cells against death-receptor-induced apoptosis may lead to higher virus production and contribute to the persistence and oncogenicity of several FLIP-encoding viruses.

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