PARN

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]

poly(A)-specific ribonuclease

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 (PubMed:10882133, PubMed:11359775, PubMed:12748283, PubMed:15175153, PubMed:9736620).
Also able to recognize and trim poly(A) tails of microRNAs such as MIR21 and H/ACA box snoRNAs (small nucleolar RNAs) leading to microRNAs degradation or snoRNA increased stability (PubMed:25049417, PubMed:22442037).

Box H/ACA RNA 3'-end processingManual Assertion Based On ExperimentIDA:UniProtKB
Female gamete generationManual Assertion Based On ExperimentTAS:ProtInc
miRNA catabolic processManual Assertion Based On ExperimentIDA:UniProtKB
ncRNA deadenylationManual Assertion Based On ExperimentIMP:BHF-UCL
Nuclear-transcribed mRNA catabolic process, nonsense-mediated decayIEA:UniProtKB-KW
Nuclear-transcribed mRNA poly(A) tail shorteningManual Assertion Based On ExperimentIBA:GO_Central
Polyadenylation-dependent snoRNA 3'-end processingManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of telomerase activityManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of telomere maintenance via telomeraseManual Assertion Based On ExperimentIMP:BHF-UCL
Regulation of telomerase RNA localization to Cajal bodyManual Assertion Based On ExperimentIMP:BHF-UCL
RNA modificationManual Assertion Based On ExperimentTAS:ProtInc
RNA phosphodiester bond hydrolysis, exonucleolyticManual Assertion Based On ExperimentIMP:BHF-UCL
Telomerase RNA stabilizationManual Assertion Based On ExperimentIMP:BHF-UCL

Nucleus
Cytoplasm
Nucleus, nucleolus
Some nuclear fraction is nucleolar.

Dyskeratosis congenita, autosomal recessive, 6 (DKCB6):
A form of dyskeratosis congenita, a rare multisystem disorder caused by defective telomere maintenance. It is characterized by progressive bone marrow failure, and the clinical triad of reticulated skin hyperpigmentation, nail dystrophy, and mucosal leukoplakia. Common but variable features include premature graying, aplastic anemia, low platelets, osteoporosis, pulmonary fibrosis, and liver fibrosis among others. Early mortality is often associated with bone marrow failure, infections, fatal pulmonary complications, or malignancy.
Pulmonary fibrosis, and/or bone marrow failure, telomere-related, 4 (PFBMFT4):
A disease associated with shortened telomeres. Pulmonary fibrosis is the most common manifestation. Other manifestations include aplastic anemia due to bone marrow failure, hepatic fibrosis, and increased cancer risk, particularly myelodysplastic syndrome and acute myeloid leukemia. Phenotype, age at onset, and severity are determined by telomere length.

Phosphorylation by MAPKAPK2, preventing GADD45A mRNA degradation after genotoxic stress.