EC Number   |
General Information |
Reference  |
|---|
   2.7.1.78 | malfunction |
Pnk1 deletion in fission yeast renders cells sensitive to camptothecin |
716975 |
| 2.7.1.78 | malfunction |
PNKP depletion in human cells renders cells sensitive to camptothecin. A small molecule inhibitor of PNKP phosphatase activity enhances the sensitivity of cells to IR and camptothecin. Enzyme mutational defects can cause neurological disorders with various symptoms, e.g. a severe neurological autosomal recessive disease characterized by microcephaly, intractable seizures and developmental delay |
716975 |
| 2.7.1.78 | more |
molecular architecture of the enzyme, overview. The mammalian enzyme preferentially phosphorylates 5'-hydroxyl termini within nicked, gapped or double-strand breaks with single-stranded 3'-overhanging ends, whereas single-stranded 5'-termini or blunt double-stranded ends are phosphorylated less efficiently. The selective recognition of the larger, double-stranded DNA substrates is effected by a broad DNA recognition groove composed of two distinct positively charged surfaces. Mechanisms of single-strand break and double-strand break repairs, and of base excision repair, overview |
716975 |
| 2.7.1.78 | more |
molecular architecture of the enzyme, overview. The mammalian enzyme preferentially phosphorylates 5'-hydroxyl termini within nicked, gapped or DSBs with single-stranded 3' overhanging ends, whereas single-stranded 5'-termini or blunt double-stranded ends are phosphorylated less efficiently. The selective recognition of the larger, double-stranded DNA substrates is effected by a broad DNA recognition groove composed of two distinct positively charged surfaces. Mechanisms of single-strand break and double-strand break repairs, and base excision repair, overview |
716975 |
| 2.7.1.78 | more |
molecular architecture of the enzyme, overview. The phage PNK DNA binding cleft forms a narrow channel leading to the conserved catalytic aspartic acid residue that accommodates single-stranded, but not double-stranded, substrates. Mechanisms of single-strand break and double-strand break repairs, overview |
716975 |
| 2.7.1.78 | physiological function |
polynucleotide kinase/phosphatase is an essential enzyme for the repair of damaged DNA termini. PNKP possesses both 5'-kinase and 3'-phosphatase activities that are frequently required for processing of single- and double-strand break termini |
716975 |
| 2.7.1.78 | malfunction |
depletion of Nol9 leads to a severe impairment of ribosome biogenesis. Upon Nol9 knockdown, specific maturation defect at the 5' end of the predominant 5.8S short-form rRNA (5.8SS) occur, possibly due to the Nol9 requirement for 5'>3' exonucleolytic trimming |
722115 |
| 2.7.1.78 | metabolism |
polynucleotide 5-kinase Nol9 is involved in ribosomal RNA processing |
722115 |
| 2.7.1.78 | physiological function |
the nonribosomal protein Nol9 is a polynucleotide 5'-kinase that sediments primarily with the pre-60S and pre-40S ribosomal particles in HeLa nuclear extracts. The polynucleotide kinase activity of Nol9 is required for processing of large subunit rRNA and efficient generation of the 5.8S and 28S rRNAs from the 32S precursor |
722115 |
| 2.7.1.78 | malfunction |
knockdown of polynucleotide kinase and aprataxin-like forkhead-associated using siRNA reduces rejoining of two incompatible I-SceI-generated DNA ends by 50% |
722727 |
