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Literature summary for 3.1.13.4 extracted from

  • Moon, D.H.; Segal, M.; Boyraz, B.; Guinan, E.; Hofmann, I.; Cahan, P.; Tai, A.K.; Agarwal, S.
    Poly(A)-specific ribonuclease (PARN) mediates 3'-end maturation of the telomerase RNA component (2015), Nat. Genet., 47, 1482-1488 .
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens O95453
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-

Synonyms

Synonyms Comment Organism
PARN
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Homo sapiens

General Information

General Information Comment Organism
malfunction mutations in the PARN gene (encoding poly(A)-specific ribonuclease) cause telomere diseases including familial idiopathic pulmonary fibrosis and dyskeratosis congenita. PARN deficiency impairs telomere maintenance. Mechanism linking PARN mutations to telomere diseases, phenotype analysis, overview Homo sapiens
physiological function poly(A)-specific ribonuclease (PARN) mediates 3'-end maturation of the telomerase RNA component. PARN is required for removal of post-transcriptionally acquired oligo(A) tails that target nuclear RNAs for degradation. Diminished TERC levels and the increased proportion of oligo(A) forms of TERC are normalized by restoring PARN, which is limiting for TERC maturation in cells. Role for PARN in the biogenesis of TERC. TERC serves as the RNA template and scaffold for the telomerxadase reverse-transcriptase holoenzyme Homo sapiens