Evidence map›Paper›PMID 26996824›Full record

ArticleNature communications2016

miR-34 activity is modulated through 5'-end phosphorylation in response to DNA damage.

David W Salzman, Kotoka Nakamura, Sunitha Nallur, Michelle T Dookwah, Chanatip Metheetrairut, Frank J Slack, Joanne B Weidhaas

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  8. The biogenesis and regulation of animal microRNAs.Nature reviews. Molecular cell biology · 2025
    Review
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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

7 authors at 2 institutions in 1 country.

David W SalzmanDepartment of Therapeutic Radiology, Yale School of Medicine, 15 York Street, New Haven, Connecticut 06502, USA.
Kotoka NakamuraDepartment of Radiation Oncology, David Geffen School of Medicine, Los Angeles, California 90024, USA.
Sunitha NallurDepartment of Therapeutic Radiology, Yale School of Medicine, 15 York Street, New Haven, Connecticut 06502, USA.
Michelle T DookwahDepartment of Therapeutic Radiology, Yale School of Medicine, 15 York Street, New Haven, Connecticut 06502, USA.
Chanatip MetheetrairutDepartment of Molecular, Cellular and Developmental Biology, Yale University, PO Box 208103, New Haven, Connecticut 06502, USA.
Frank J SlackDepartment of Molecular, Cellular and Developmental Biology, Yale University, PO Box 208103, New Haven, Connecticut 06502, USA.
Joanne B WeidhaasDepartment of Radiation Oncology, David Geffen School of Medicine, Los Angeles, California 90024, USA.
Yale University · USUniversity of California, Los Angeles · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
MicroRNAs in agingR01AG033921 · NIA · YALE UNIVERSITY · PI SLACK, FRANK J. · 2009 to 2018
$3.3M
MicroRNAs to Understand Cause and Outcome in Breast CancerR01CA157749 · NCI · YALE UNIVERSITY · PI SLACK, FRANK J., WEIDHAAS, JOANNE B · 2012 to 2016
$1.7M
Let-7 microRNAs in Lung Cancer: Altering Growth and RadioresistanceR01CA131301 · NCI · YALE UNIVERSITY · PI SLACK, FRANK J., WEIDHAAS, JOANNE B · 2009 to 2013
$1.7M
NCI NIH HHS CA131301NCI NIH HHS CA157749NCI NIH HHS P30 CA016042NCI NIH HHS R01 CA131301NCI NIH HHS R01 CA157749NIA NIH HHS AG033921NIA NIH HHS R01 AG033921
6 · The paper itself

Abstract

MicroRNA (miRNA) expression is tightly regulated by several mechanisms, including transcription and cleavage of the miRNA precursor RNAs, to generate a mature miRNA, which is thought to be directly correlated with activity. MiR-34 is a tumour-suppressor miRNA important in cell survival, that is transcriptionally upregulated by p53 in response to DNA damage. Here, we show for the first time that there is a pool of mature miR-34 in cells that lacks a 5'-phosphate and is inactive. Following exposure to a DNA-damaging stimulus, the inactive pool of miR-34 is rapidly activated through 5'-end phosphorylation in an ATM- and Clp1-dependent manner, enabling loading into Ago2. Importantly, this mechanism of miR-34 activation occurs faster than, and independently of, de novo p53-mediated transcription and processing. Our study reveals a novel mechanism of rapid miRNA activation in response to environmental stimuli occurring at the mature miRNA level.

Indexed as

Argonaute ProteinsAtaxia Telangiectasia Mutated ProteinsCell LineDNA DamageGene Expression RegulationHumansMicroRNAsNuclear ProteinsPhosphorylationPhosphotransferasesTranscription FactorsTumor Suppressor Protein p53AGO2 protein, humanArgonaute ProteinsAtaxia Telangiectasia Mutated ProteinsCLP1 protein, humanMicroRNAsMIRN34 microRNA, humanNuclear ProteinsPhosphotransferasesTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID26996824
PMCPMC4802117
OpenAlexW2305644015

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.