2.7.7.8: polyribonucleotide nucleotidyltransferase
This is an abbreviated version!
For detailed information about polyribonucleotide nucleotidyltransferase, go to the full flat file.
Word Map on EC 2.7.7.8
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2.7.7.8
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rnase
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exoribonuclease
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polya
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ribonuclease
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polymerization
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polyadenylation
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phosphorolysis
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degradosome
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helicase
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exonuclease
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exonucleolytic
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stem-loop
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luteus
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micrococcus
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5'-diphosphate
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rna-binding
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kh
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hfq
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oligoribonucleotides
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rna-degrading
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heteropolymeric
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antibioticus
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dead-box
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lysodeikticus
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primer-independent
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synthesis
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molecular biology
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medicine
- 2.7.7.8
- rnase
- exoribonuclease
- polya
- ribonuclease
- polymerization
-
polyadenylation
-
phosphorolysis
-
degradosome
- helicase
-
exonuclease
-
exonucleolytic
-
stem-loop
- luteus
- micrococcus
- 5'-diphosphate
-
rna-binding
- kh
- hfq
- oligoribonucleotides
-
rna-degrading
-
heteropolymeric
- antibioticus
-
dead-box
- lysodeikticus
-
primer-independent
- synthesis
- molecular biology
- medicine
Reaction
Synonyms
AtcpPNPase, AtmtPNPase, chloroplast PNPase, cpPNPase, hPNPase(old-35), hPNPaseold-35, nucleoside diphosphate:polynucleotidyl transferase, nucleotidyltransferase, polyribonucleotide, PNP, PNPase, PNPT1, polynucleotide phosphorylase, polyribonucleotide phosphorylase, RNase PH
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Application on EC 2.7.7.8 - polyribonucleotide nucleotidyltransferase
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APPLICATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
medicine
molecular biology
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targeted overexpression of hPNPase represents a strategy to selectively downregulate RNA expression and consequently intervene in a variety of pathophysiological conditions
synthesis
at the optimal temperature, polynucleotide phosphorylase completely destroys RNAs that possess even a very stable intramolecular secondary structure, but leaves intact RNAs whose 3' end is protected by chemical modification or by hybridization with a complementary oligonucleotide. This allows individual RNAs to be isolated from heterogeneous populations by degrading unprotected species. If oligonucleotide is hybridized to an internal RNA segment, the Tth polynucelotide phosphorylase stalls eight nucleotides downstream of that segment. This allows any arbitrary 5'-terminal fragment of RNA to be prepared with a precision similar to that of run-off transcription, but without the need for a restriction site
medicine
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depletion of enzyme by RNAi approach or overexpression of c-myc protects melanoma cells from interferon-beta mediated grwoth inhibition. Targeted overexpression of enzyme as a therapeutic strategy for c-myc overexpressing and interferon-beta resistant tumors
medicine
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the apoptosis-inducing activity of polynucleotide phosphorylase is mediated by activation of double-stranded RNA-dependent protein kinase. Activation of RNA-dependent protein kinase by polynucleotide phosphorylase precedes phosphorylation of eukaryotic initiation factor-2A and induction of growth arrest and DNA damage-inducible gene 153, GADD153, that culminates in the shutdown of protein synthesis and apoptosis. Activation of RNA-dependent protein kinase by polynucleotide phosphorylase also instigates down-regulation of the antiapoptotic protein Bcl-xL. A dominant-negative inhibitor of RNA-dependent protein kinase, as well as GADD153 antisense or bcl-xL overexpression, effectively inhibits apoptosis induction by polynucleotide phosphorylase
medicine
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the promoter of Progression Elevated Gene-3 functions selectively in a diverse array of human cancer cells. An adenovirus constructed with the Progression Elevated Gene-3 promoter driving expression of polyribonucleotide phosphorylase containing a C-terminal hemaglutinin-tag induces robust transgene expression, growth suppression, apoptosis, and cell-cycle arrest in a broad panel of pancreatic cancer cells, with minimal effects in normal immortalized pancreatic cells. Expression correlates with arrest in the G2/M phase of the cell cycle and up-regulation of the cyclin-dependent kinase inhibitors p21CIP1/WAF-1/MDA-6 and p27KIP1. In a nude mouse xenograft model,construct injections effectively inhibit growth of human pancreatic cancer cells in vivo
medicine
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targeted overexpression of hPNPaseold-35 might provide an effective therapeutic strategy for miR-221-overexpressing and IFN-resistant tumors, such as melanoma
