Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.27.5 (RNase)
 17,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

2',5'-adenylate oligonucleotide (2-5A)-dependent RNase and 2-5A-synthetase are two enzymes of the 2-5A system strongly implicated in the basal control of RNA decay of both interferon-treated and untreated cells. RNase is activated by a 2-5A produced by 2-5A-synthetase, both enzymes being overexpressed by type I-interferon (alpha/beta). We described here for the first time a cell line completely deficient in RNase and its mRNA, while p69 2-5A-synthetase was normally interferon alpha/beta-induced. The complete absence of this RNase in human hepatoma cells (HepG2) was shown using three different methods based on the binding of a [32P]-labeled 2-5A probe of high specific activity to its binding site. Negative Western blotting assay with a specific monoclonal antibody correlated the previous findings. RNase-specific mRNA was not detectable even after treatment of cells with 1000 units/ml of interferon alpha/beta. This is not due to a mutation of the gene because an intronless genomic DNA sequence encoding 2-5A-binding site was cloned and expressed. It is likely that the expression of 2-5A-dependent RNase was impaired at the transcriptional level while having the known IFN alpha/beta-transcriptional regulatory factors as revealed by induction of p69 2-5A-synthetase gene. This may account for a differential activation of 2-5A-dependent RNase and 2-5A-synthetase genes by type I-interferon, and suggests that other members of regulatory transcription factors, different from IRF-1 and STAT proteins, may participate in two different interferon alpha/beta signaling pathways.
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PMID:Lack of 2',5'-oligoadenylate-dependent RNase expression in the human hepatoma cell line HepG2. 956

Small interfering RNAs (siRNAs) and microRNAs (miRNAs) are processed by the ribonuclease Dicer from distinct precursors, double-stranded RNA (dsRNA) and hairpin RNAs, respectively, although either may guide RNA silencing via a similar complex. The siRNA pathway is antiviral, whereas an emerging role for miRNAs is in the control of development. Here, we describe a virulence factor encoded by turnip yellow mosaic virus, p69, which suppresses the siRNA pathway but promotes the miRNA pathway in Arabidopsis thaliana. p69 suppression of the siRNA pathway is upstream of dsRNA and is as effective as genetic mutations in A. thaliana genes involved in dsRNA production. Possibly as a consequence of p69 suppression, p69-expressing plants contained elevated levels of a Dicer mRNA and of miRNAs as well as a correspondingly enhanced miRNA-guided cleavage of two host mRNAs. Because p69-expressing plants exhibited disease-like symptoms in the absence of viral infection, our findings suggest a novel mechanism for viral virulence by promoting the miRNA-guided inhibition of host gene expression.
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PMID:Viral virulence protein suppresses RNA silencing-mediated defense but upregulates the role of microrna in host gene expression. 1510 Mar 97