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The role of 2′-5′ oligoadenylate-activated ribonuclease L in apoptosis
被引:151
作者:
Castelli, JC
Hassel, BA
Maran, A
Paranjape, J
Hewitt, JA
Li, XL
Hsu, YT
Silverman, RH
Youle, RJ
[1
]
机构:
[1] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA
[2] Cleveland Clin Fdn, Res Inst, Dept Canc Biol, Cleveland, OH 44195 USA
[3] Univ Maryland, Baltimore Canc Ctr, Dept Immunol & Microbiol, Baltimore, MD 21201 USA
关键词:
programmed cell death;
interferon;
viruses;
staurosporine;
diethylmaleate;
D O I:
10.1038/sj.cdd.4400352
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
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 com prised of 2'-5' oligoadenylate synthetase (GAS), 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.
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页码:313 / 320
页数:8
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