Linked Life Data

15522195

Source:http://linkedlifedata.com/resource/pubmed/id/15522195

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-11-3
pubmed:abstractText
Accelerated decrease in the levels of mitochondrial DNA-encoded mRNA (mt-mRNA) occurs in neuronal cells exposed either to the excitatory amino acid, glutamate or to the sodium ionophore, monensin, suggesting a role of mitochondrial RNase(s) on the stability of mt-mRNAs. Here we report that in mouse embryo fibroblasts that are devoid of the interferon-regulated RNase, RNase-L, the monensin-induced decrease in the half-life of mt-mRNA was reduced. In monensin (250 nM)-treated RNase-L(+/+) cells the average half-life of mt-mRNA, determined after termination of transcription with actinomycin D, was found to be 3h, whereas in monensin-treated RNase-L(-/-) cells the half-life of mt-mRNA was >6h. In contrast, the stability of nuclear DNA-encoded beta-actin mRNA was unaffected. Induction of RNase-L expression in mouse 3T3 fibroblasts further decreased the monensin-induced reduction in mt-mRNA half-life to 1.5h. The results indicate that the RNase-L-dependent decrease in mtDNA-encoded mRNA transcript levels occurs through a decrease in the half-life of mt-mRNA, and that RNase-L may play a role in the stability of mt-mRNA.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
325
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
18-23
pubmed:dateRevised
2011-6-17
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
RNase-L regulates the stability of mitochondrial DNA-encoded mRNAs in mouse embryo fibroblasts.
pubmed:affiliation
Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA. kchandra@anethlab.umm.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't