ArticleThe Journal of clinical investigation2015
mRNA deadenylation and telomere disease.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Multiple bilateral hip fractures in a patient with dyskeratosis congenita caused by a novel mutation in the PARN gene.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2021Article
- Connections between 3' end processing and DNA damage response: Ten years later.Wiley interdisciplinary reviews. RNA · 2020Review
- Impaired telomere integrity and rRNA biogenesis in PARN-deficient patients and knock-out models.EMBO molecular medicine · 2019Article
- The Interplay between the RNA Decay and Translation Machinery in Eukaryotes.Cold Spring Harbor perspectives in biology · 2018Review
- A feedback mechanism between PLD and deadenylase PARN for the shortening of eukaryotic poly(A) mRNA tails that is deregulated in cancer cells.Biology open · 2017Article
- Poly(A)-specific ribonuclease (PARN) mediates 3'-end maturation of the telomerase RNA component.Nature genetics · 2015Article
Corrections and comments
- Comment on
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Dyskeratosis congenita (DC) is an inherited BM failure disorder that is associated with mutations in genes involved with telomere function and maintenance; however, the genetic cause of many instances of DC remains uncharacterized. In this issue of the JCI, Tummala and colleagues identify mutations in the gene encoding the poly(A)-specific ribonuclease (PARN) in individuals with a severe form of DC in three different families. PARN deficiency resulted in decreased expression of genes required for telomere maintenance and an aberrant DNA damage response, including increased levels of p53. Together, the results of this study support PARN as a DC-associated gene and suggest a potential link between p53 and telomere shortening.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.