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	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	
2.7.1.78	malfunction	mutations lead to a loss of enzyme interaction with the tRNA splicing endonuclease complex, largely reduced pretRNA cleavage activity, and accumulation of linear tRNA introns. The affected individuals develop severe motor-sensory defects, cortical dysgenesis, and microcephaly	729562	
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	malfunction	polynucleotide kinase Grc3 depletion results in rRNA processing defects	739186	
2.7.1.78	malfunction	the lack of CLP1 kinase activity leads to progressive motor neuron loss and accumulation of novel 5' leader-5' exon tRNA fragments	729174	
2.7.1.78	metabolism	polynucleotide 5-kinase Nol9 is involved in ribosomal RNA processing	722115	
2.7.1.78	metabolism	the enzyme is part of the Pnkp-Hen1 RNA repair pathway, overview	723764	
2.7.1.78	metabolism	the enzyme is required for 60S ribosomal particles synthesis	739186