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Death effector domain-containing herpesvirus and poxvirus proteins inhibit both Fas- and TNFR1-induced apoptosis.
- Source :
-
Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 1997 Feb 18; Vol. 94 (4), pp. 1172-6. - Publication Year :
- 1997
-
Abstract
- To identify novel antiapoptotic proteins encoded by DNA viruses, we searched viral genomes for proteins that might interfere with Fas and TNFR1 apoptotic signaling pathways. We report here that equine herpesvirus type 2 E8 protein and molluscum contagiosum virus MC159 protein both show sequence similarity to the death effector domains (DEDs) of the Fas/TNFR1 signaling components FADD and caspase-8. Yeast two-hybrid analysis revealed that E8 protein interacted with the caspase-8 prodomain whereas MC159 protein interacted with FADD. Furthermore, expression of either E8 protein or MC159 protein protected cells from Fas- and TNFR1-induced apoptosis indicating that certain herpesviruses and poxviruses use DED-mediated interactions to interfere with apoptotic signaling pathways. These findings identify a novel control point exploited by viruses to regulate Fas- and TNFR1-mediated apoptosis.
- Subjects :
- Amino Acid Sequence
Base Sequence
Carrier Proteins metabolism
Cysteine Endopeptidases metabolism
Fas-Associated Death Domain Protein
Herpesviridae
Models, Biological
Molecular Sequence Data
Molluscum contagiosum virus
Protein Binding
Receptors, Tumor Necrosis Factor, Type I
Sequence Homology, Amino Acid
Signal Transduction
Adaptor Proteins, Signal Transducing
Antigens, CD metabolism
Apoptosis physiology
DNA Viruses
Receptors, Tumor Necrosis Factor metabolism
Viral Proteins metabolism
fas Receptor metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0027-8424
- Volume :
- 94
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Proceedings of the National Academy of Sciences of the United States of America
- Publication Type :
- Academic Journal
- Accession number :
- 9037025
- Full Text :
- https://doi.org/10.1073/pnas.94.4.1172