Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

PARN Modulates Y RNA Stability and Its 3'-End Formation.

Molecular and cellular biology - 15 Oct 2017

Shukla Siddharth, Parker Roy

Abstract excerpt

Loss-of-function mutations in 3'-to-5' exoribonucleases have been implicated in hereditary human diseases. For example, PARN mutations cause a severe form of dyskeratosis congenita (DC), wherein PARN deficiency leads to human telomerase RNA instability. Since the DC phenotype in PARN patients is even more severe than that of loss-of-function alleles in telomerase components, we hypothesized that PARN would also...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alleles
Share to Dyskeratosis Congenita
Share to Exoribonucleases

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to HeLa Cells

Share to Phenotype

Share to RNA Stability

Share to Telomerase

Source

Open in PubMed Open full text

Identifiers

PMID: 28760775
DOI: 10.1128/MCB.00264-17
PMCID: PMC5615183

Genes

PARN

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

PARN Modulates Y RNA Stability and Its 3'-End Formation.PMID 28760775Read ↗

Poly(A)-specific ribonuclease (PARN) mediates 3'-end maturation of the telomerase RNA component.Semantic proximity Read ↗

Posttranscriptional modulation of TERC by PAPD5 inhibition rescues hematopoietic development in dyskeratosis congenitaSemantic proximity Read ↗

Poly(A)-specific ribonuclease deficiency impacts telomere biology and causes dyskeratosis congenita.Semantic proximity Read ↗

Domain specific mutations in dyskerin disrupt 3' end processing of scaRNA13.Semantic proximity Read ↗

Posttranscriptional manipulation of TERC reverses molecular hallmarks of telomere disease.Semantic proximity Read ↗

H/ACA small RNA dysfunctions in disease reveal key roles for noncoding RNA modifications in hematopoietic stem cell differentiation.Semantic proximity Read ↗

Chemical inhibition of PAPD5/7 rescues telomerase function and hematopoiesis in dyskeratosis congenita.Semantic proximity Read ↗

From incomplete penetrance with normal telomere length to severe disease and telomere shortening in a family with monoallelic and biallelic PARN pathogenic variantsSemantic proximity Read ↗

Bone marrow failure and developmental delay caused by mutations in poly(A)-specific ribonuclease (PARN).Semantic proximity Read ↗

A nuclear RNA degradation code for eukaryotic transcriptome surveillanceSemantic proximity Read ↗

High-throughput siRNA screening reveals functional interactions and redundancies of human processive exoribonucleasesSemantic proximity Read ↗

TOE1 acts as a 3′ exonuclease for telomerase RNA and regulates telomere maintenanceSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.