EC Number   |
General Information |
Reference |
|---|
   3.1.13.4 | evolution |
PARN is a member of the DEDD family of 3'-to-5' exonucleases with a marked nucleotide preference towards A |
752164 |
| 3.1.13.4 | malfunction |
AGO-APP from parental or PARN knockout cells enrich the miRNAs to a similar extent, without altering the overall length distribution of the miRNA isoforms, suggesting that PARN-mediated trimming does not affect the interaction of miRNAs with AGO proteins |
752164 |
| 3.1.13.4 | malfunction |
depletion of poly(A)-specific ribonuclease (PARN) inhibits proliferation of human gastric cancer cells by blocking cell cycle progression. PARN depletion leads to cell cycle arrest by upregulating p21 expression, stabilizes the p21 mRNA (one of the key regulators in cell growth and survival), and promotes cell death, but does not affect the formation of RNA granules |
749952 |
| 3.1.13.4 | malfunction |
knockdown of PARN or exogenous expression of an enzyme-dead PARN mutant (D28A) accumulates 18S-E in both the cytoplasm and nucleus. Expression of D28A accumulates 18S-E in Bystin-associated pre-40S particles. RNase H-based fragmentation analysis and 3'-sequence analysis of 18S-E species present in cells expressing wild-type PARN or D28A, overview |
751740 |
| 3.1.13.4 | malfunction |
knocking down ribosome biogenesis factors (RBFs) involved in the large subunit pathway (LSG1 and eIF6) has no effect on PARN localization. Co-depletion of PARN and NOB1 yields a much stronger accumulation of 18S-EFL species than the sole knockdown of PARN. This suggests that NOB1 can also cleave untrimmed 18S-E pre-rRNAs, albeit less efficiently. In accordance with this assumption, overexpression of NOB1 in PARN-depleted cells leads to a decreased amount of 18S-EFL pre-rRNA |
751744 |
| 3.1.13.4 | malfunction |
mice lacking the Noc gene display resistance to diet-induced obesity and hepatic steatosis, due in part to reduced lipid trafficking in the small intestine |
758517 |
| 3.1.13.4 | malfunction |
mutations in PARN in patients with haematological and neurological manifestations. Large monoallelic deletions in PARN in four patients with developmental delay or mental illness. One patient in particular has a severe neurological phenotype, central hypomyelination and bone marrow failure. This patient has an additional missense mutation on the non-deleted allele and severely reduced PARN protein and deadenylation activity. Cells from this patient have impaired oligoadenylation of specific H/ACA box small nucleolar RNAs. Importantly, PARN-deficient patient cells manifest short telomeres and an aberrant ribosome profile similar to those described in some variants of dyskeratosis congenita. Knocking down PARN in human marrow cells impaires haematopoiesis. Biallelic mutations in PARN results in severely reduced protein level. PARN-deficient patient cells manifest PARN-associated defects in snoRNA and scaRNA trimming and aberrant ribosome profile. Phenotypes, detailed overview |
751289 |
| 3.1.13.4 | 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 |
751677 |
| 3.1.13.4 | malfunction |
Noc knock-out (Noc-/-) mice exhibit no obvious abnormalities in development or reproduction, however, they exhibit striking metabolic phenotypes when fed a High-Fat Diet (HFD). This diet causes wild-type mice to become obese, but the Noc-/- mice remain lean although they do not exhibit increased activity or reduced food intake |
756072 |
| 3.1.13.4 | metabolism |
3' ends of metazoan microRNAs (miRNAs) are initially defined by the RNase III enzymes during maturation, but subsequently experience extensive modifications by several enzymatic activities. For example, terminal nucleotidyltransferases (TENTs) elongate miRNAs by adding one or a few nucleotides to their 3' ends, which occasionally leads to differential regulation of miRNA stability or function. Poly(A)-specific ribonuclease (PARN) forms the 3' ends of miRNAs in human cells |
752164 |
