Aliases for PARN Gene
External Ids for PARN Gene
Previous GeneCards Identifiers for PARN Gene
The protein encoded by this gene is a 3'-exoribonuclease, with similarity to the RNase D family of 3'-exonucleases. It prefers poly(A) as the substrate, hence, efficiently degrades poly(A) tails of mRNAs. Exonucleolytic degradation of the poly(A) tail is often the first step in the decay of eukaryotic mRNAs. This protein is also involved in silencing of certain maternal mRNAs during oocyte maturation and early embryonic development, as well as in nonsense-mediated decay (NMD) of mRNAs that contain premature stop codons. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2008]
GeneCards Summary for PARN Gene
PARN (Poly(A)-Specific Ribonuclease) is a Protein Coding gene. Diseases associated with PARN include Pulmonary Fibrosis And/Or Bone Marrow Failure, Telomere-Related, 4 and Dyskeratosis Congenita, Autosomal Recessive 6. Among its related pathways are CDK-mediated phosphorylation and removal of Cdc6 and Translational Control. GO annotations related to this gene include nucleic acid binding and RNA binding. An important paralog of this gene is PNLDC1.
UniProtKB/Swiss-Prot for PARN Gene
3-exoribonuclease that has a preference for poly(A) tails of mRNAs, thereby efficiently degrading poly(A) tails. Exonucleolytic degradation of the poly(A) tail is often the first step in the decay of eukaryotic mRNAs and is also used to silence certain maternal mRNAs translationally during oocyte maturation and early embryonic development. Interacts with both the 3-end poly(A) tail and the 5-end cap structure during degradation, the interaction with the cap structure being required for an efficient degradation of poly(A) tails. Involved in nonsense-mediated mRNA decay, a critical process of selective degradation of mRNAs that contain premature stop codons. Also involved in degradation of inherently unstable mRNAs that contain AU-rich elements (AREs) in their 3-UTR, possibly via its interaction with KHSRP. Probably mediates the removal of poly(A) tails of AREs mRNAs, which constitutes the first step of destabilization.