Evidence map›Paper›PMID 26001796›Full record

ArticleRNA (New York, N.Y.)2015

DcpS is a transcript-specific modulator of RNA in mammalian cells.

Mi Zhou, Sophie Bail, Heather L Plasterer, James Rusche, Megerditch Kiledjian

Open access · bronzeAbstract read
In one paragraph

Article in RNA (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. Small molecule targeting of RNA structures in neurological disorders.Annals of the New York Academy of Sciences · 2020
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Cytoplasmic mRNA turnover and ageing.Mechanisms of ageing and development · 2015
    Review
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Mi ZhouDepartment of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854, USA.
Sophie BailDepartment of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854, USA.
Heather L PlastererRepligen Corporation, Waltham, Massachusetts 02453, USA.
James RuscheRepligen Corporation, Waltham, Massachusetts 02453, USA.
Megerditch KiledjianDepartment of Cell Biology and Neuroscience, Rutgers University, Piscataway, New Jersey 08854, USA kiledjian@biology.rutgers.edu.
Rutgers, The State University of New Jersey · USRepligen (United States) · US

Funding

Regulation of Mammalian mRNA DecayR01GM067005 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI KILEDJIAN, MEGERDITCH · 2004 to 2022
$5.5M
NIGMS NIH HHS GM067005NIGMS NIH HHS R01 GM067005
6 · The paper itself

Abstract

The scavenger decapping enzyme DcpS is a multifunctional protein initially identified by its property to hydrolyze the resulting cap structure following 3' end mRNA decay. In Saccharomyces cerevisiae, the DcpS homolog Dcs1 is an obligate cofactor for the 5'-3' exoribonuclease Xrn1 while the Caenorhabditis elegans homolog Dcs-1, facilitates Xrn1 mediated microRNA turnover. In both cases, this function is independent of the decapping activity. Whether DcpS and its decapping activity can affect mRNA steady state or stability in mammalian cells remains unknown. We sought to determine DcpS target genes in mammalian cells using a cell-permeable DcpS inhibitor compound, RG3039 initially developed for therapeutic treatment of spinal muscular atrophy. Global mRNA levels were examined following DcpS decapping inhibition with RG3039. The steady-state levels of 222 RNAs were altered upon RG3039 treatment. Of a subset selected for validation, two transcripts that appear to be long noncoding RNAs HS370762 and BC011766, were dependent on DcpS and its scavenger decapping catalytic activity and referred to as DcpS-responsive noncoding transcripts (DRNT) 1 and 2, respectively. Interestingly, only the increase in DRNT1 transcript was accompanied with an increase of its RNA stability and this increase was dependent on both DcpS and Xrn1. Importantly, unlike in yeast where the DcpS homolog is an obligate cofactor for Xrn1, stability of additional Xrn1 dependent RNAs were not altered by a reduction in DcpS levels. Collectively, our data demonstrate that DcpS in conjunction with Xrn1 has the potential to regulate RNA stability in a transcript-selective manner in mammalian cells.

Indexed as

Base SequenceCell LineDNA PrimersEndoribonucleasesHumansQuinazolinesReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerRNA StabilityRNA, Untranslated5-((1-(2,6-dichlorobenzyl)piperidin-4-yl)methoxy)quinazoline-2,4-diamineDcpS protein, humanDNA PrimersEndoribonucleasesQuinazolinesRNA, MessengerRNA, UntranslatedDcpSlncRNARNA decayXRN1

Identifiers

PMID26001796
PMCPMC4478349
OpenAlexW2108400024

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.