The role of 2′-5′ oligoadenylate-activated ribonuclease L in apoptosis
| Autor: | Avudaiappan Maran, Jayashree M. Paranjape, Judith A. Hewitt, Richard J. Youle, Yi-Te Hsu, Joann C. Castelli, Robert H. Silverman, Xiaoling Li, Bret A. Hassel |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Programmed cell death
RNase P bcl-X Protein Gene Expression Apoptosis Cell Line Mice Bcl-2-associated X protein Interferon Proto-Oncogene Proteins Endoribonucleases medicine Animals Humans Enzyme Inhibitors Molecular Biology bcl-2-Associated X Protein Cell Nucleus Oligoribonucleotides biology Adenine Nucleotides Chemistry 2'-5'-Oligoadenylate Maleates 3T3 Cells Hydrogen Peroxide Cell Biology Transfection Staurosporine Molecular biology Genes bcl-2 Cell biology Proto-Oncogene Proteins c-bcl-2 Protein Biosynthesis Mutation biology.protein K562 Cells Ribonuclease L medicine.drug |
| Zdroj: | Cell Death & Differentiation. 5:313-320 |
| ISSN: | 1476-5403 1350-9047 |
| Popis: | Apoptosis of viral infected cells appears to be one defense strategy to limit viral infection. Interferon can also confer viral resistance by the induction of the 2-5A system comprised of 2'-5' oligoadenylate synthetase (OAS), and RNase L. Since rRNA is degraded upon activation of RNase L and during apoptosis and since both of these processes serve antiviral functions, we examined the role RNase L may play in cell death. Inhibition of RNase L activity, by transfection with a dominant negative mutant, blocked staurosporine-induced apoptosis of NIH3T3 cells and SV40-transformed BALB/c cells. In addition, K562 cell lines expressing inactive RNase L were more resistant to apoptosis induced by decreased glutathione levels. Hydrogen peroxide-induced death of NIH3T3 cells did not occur by apoptosis and was not dependent upon active RNAse L. Apoptosis regulatory proteins of the Bcl-2 family did not exhibit altered expression levels in the absence of RNase L activity. RNase L is required for certain pathways of cell death and may help mediate viral-induced apoptosis. |
| Databáze: | OpenAIRE |
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