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Results show that PARN deadenylase activity is regulated by the phosphorylated form of Nucleolin.
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Studies suggest that the effects of poly(A)-specific ribonuclease (PARN) mutations on telomere length are likely indirect and may lead to telomere shortening that less perfectly cosegregates with heterozygous mutations.
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Pulmonary fibrosis patients with mutations in telomerase reverse transcriptase, telomerase RNA component, regulator of telomere elongation helicase 1 and poly(A)-specific ribonuclease were identified and clinical data were analysed. Genetic mutations in telomere related genes lead to a variety of interstitial lung disease diagnoses that are universally progressive.
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PARN polyadenylates the 3' end of telomerase RNA component (known as TERC or hTR), which serves as the template for telomerase reverse transcriptase-mediated telomere replication.
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PARN is a new component of the ribosome biogenesis machinery in human cells.
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provide evidence that PARN can also deadenylate the U6 and RMRP RNAs without affecting their levels
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poly(A)-specific ribonuclease (PARN) participates in steps leading to 18S pre-rRNA maturation in human cells
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we found a polyadenylation-dependent 3' end maturation pathway for the human telomerase RNA that relies on the nuclear poly(A)-binding protein PABPN1 and the poly(A)-specific RNase PARN.
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PARN increased telomerase RNA component levels by deadenylating telomerase RNA component, thereby limiting its degradation by EXOSC10.
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Large monoallelic mutations of PARN can cause developmental/mental illness. Biallelic PARN mutations cause severe bone marrow failure and central hypomyelination.
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results highlight the clinical significance of PARN and NOC on the survival in SCC diagnosed patients.
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Mutations in the PARN gene cause dyskeratosis congenital.
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The results indicate that the cellular level of miR-122 is determined by the balance between the opposing effects of GLD-2 and PARN/CUGBP1 on the metabolism of its 3'-terminus.
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3 families with dyskeratosis congenita had key domain mutations in PARN shortening telomeres, reducing deadenylation, and downregulating TERC, DKC1, RTEL1, and TERF1.
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PARN and RTEL1 mutation carriers had shortened leukocyte telomere lengths.
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poly(A)-specific ribonuclease (PARN) was upregulated in gastric tumor tissues and gastric cancer cell lines MKN28 and AGS.
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Both R3H and RRM domains were essential for the high affinity of long poly(A) substrate.
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poly(A) polymerase Gld2, deadenylase PARN, and translation inhibitory factor neuroguidin (Ngd) are components of a dendritic CPEB-associated polyadenylation apparatus
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The atomic force microscopy images of single PARN molecules reveal compact ellipsoidal dimers (10.9 x 7.6 x 4.6nm).
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PARN harbors specificity for adenosine recognition in its active site and that the nucleotides surrounding the scissile bond are critical for adenosine recognition.