Poly A Specific Ribonuclease Proteine (PARN)

Human Poly A Specific Ribonuclease (PARN) Interaktionspartner

1. PARN-mediated shortening is pervasive across most miRNAs and appears to be a conserved mechanism contributing to the 3' end formation of vertebrate miRNAs. Our findings add miRNAs to the expanding list of noncoding RNAs whose 3' end formation depends on PARN.

2. Processing of 3' telomerase RNA occurs in two steps with longer forms first being trimmed by RRP6 and shorter forms then being processed by PARN.

3. Results show that PARN deadenylase activity is regulated by the phosphorylated form of Nucleolin.

4. 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.

5. 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.

6. 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.

7. PARN is a new component of the ribosome biogenesis machinery in human cells.

8. provide evidence that PARN can also deadenylate the U6 and RMRP RNAs without affecting their levels

9. poly(A)-specific ribonuclease (PARN) participates in steps leading to 18S pre-rRNA maturation in human cells

10. 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.

11. PARN increased telomerase RNA component levels by deadenylating telomerase RNA component, thereby limiting its degradation by EXOSC10.

12. Large monoallelic mutations of PARN can cause developmental/mental illness. Biallelic PARN mutations cause severe bone marrow failure and central hypomyelination.

13. results highlight the clinical significance of PARN and NOC on the survival in SCC diagnosed patients.

14. Mutations in the PARN gene cause dyskeratosis congenital.

15. 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.

16. 3 families with dyskeratosis congenita had key domain mutations in PARN shortening telomeres, reducing deadenylation, and downregulating TERC, DKC1, RTEL1, and TERF1.

17. PARN and RTEL1 mutation carriers had shortened leukocyte telomere lengths.

18. poly(A)-specific ribonuclease (PARN) was upregulated in gastric tumor tissues and gastric cancer cell lines MKN28 and AGS.

19. Both R3H and RRM domains were essential for the high affinity of long poly(A) substrate.

20. poly(A) polymerase Gld2, deadenylase PARN, and translation inhibitory factor neuroguidin (Ngd) are components of a dendritic CPEB-associated polyadenylation apparatus

Mouse (Murine) Poly A Specific Ribonuclease (PARN) Interaktionspartner

1. these data indicate that PARN modulates decay of a defined set of mRNAs in mammalian cells and implicate this deadenylase in coordinating control of genes required for cell movement.

2. poly(A) polymerase Gld2, deadenylase PARN, and translation inhibitory factor neuroguidin (Ngd) are components of a dendritic CPEB-associated polyadenylation apparatus

3. Solution structures of the cap-binding domain of mouse PARN with and without the m(7)GpppG cap analog reveal a novel cap-binding mode.

4. A modeled PARN, which shows that the RRM domain from one subunit and the R3H domain from the other subunit enclose the active site.