Evidence map›Paper›PMID 24990949›Full record

ArticleThe Journal of biological chemistry2014

Suppression of the DHX9 helicase induces premature senescence in human diploid fibroblasts in a p53-dependent manner.

Teresa Lee, Domenic Di Paola, Abba Malina, John R Mills, Amina Kreps, Frank Grosse, Hengli Tang, Maria Zannis-Hadjopoulos, Ola Larsson, Jerry Pelletier

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 45 citations in OpenAlex.

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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

10 authors at 4 institutions in 4 countries.

Teresa LeeDepartment of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada.
Domenic Di PaolaDepartment of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada.
Abba MalinaDepartment of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada.
John R MillsDepartment of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada.
Amina KrepsDepartment of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada.
Frank GrosseLeibniz Institute for Age Research, Fritz Lipmann Institute, Jena D-07745, Germany.
Hengli TangDepartment of Biological Science, Florida State University, Tallahassee, Florida 32306.
Maria Zannis-HadjopoulosDepartment of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada,; Department of Oncology, McGill University, Montreal, Quebec H3A 1A3, Canada; The Rosalind and Morris Goodman Cancer Research Center, McGill University, Montreal, Quebec H3A 1A3, Canada, and.
Ola LarssonDepartment of Oncology-Pathology, Karolinska Institute, Stockholm 171 77, Sweden.
Jerry PelletierDepartment of Biochemistry, McGill University, Montreal, Quebec H3G 1Y6, Canada,; Department of Oncology, McGill University, Montreal, Quebec H3A 1A3, Canada; The Rosalind and Morris Goodman Cancer Research Center, McGill University, Montreal, Quebec H3A 1A3, Canada, and. Electronic address: jerry.pelletier@mcgill.ca.
McGill University · CAFlorida State University · USKarolinska Institutet · SELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DE

Funding

Vascular targeted pan PI-3 kinase inhibitor prodrug, SF1126 for glioma therapyR01CA094233 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DURDEN, DONALD · 2002 to 2012
$2.4M
Targeting the DHX9 Helicase for Small Molecule Probe DiscoveryR01CA163291 · NCI · MCGILL UNIVERSITY · PI PELLETIER, JERRY · 2012 to 2014
$454k
Vascular targeted pan PI-3kinase inhibitor prodrug, SF1126 for glioma therapy.R56CA094233 · NCI · EMORY UNIVERSITY · PI DURDEN, DONALD · 2008 to 2008
$224k
CIHR MOP-115126NCI NIH HHS CA94233NCI NIH HHS R01 CA163291
6 · The paper itself

Abstract

DHX9 is an ATP-dependent DEXH box helicase with a multitude of cellular functions. Its ability to unwind both DNA and RNA, as well as aberrant, noncanonical polynucleotide structures, has implicated it in transcriptional and translational regulation, DNA replication and repair, and maintenance of genome stability. We report that loss of DHX9 in primary human fibroblasts results in premature senescence, a state of irreversible growth arrest. This is accompanied by morphological defects, elevation of senescence-associated β-galactosidase levels, and changes in gene expression closely resembling those encountered during replicative (telomere-dependent) senescence. Activation of the p53 signaling pathway was found to be essential to this process. ChIP analysis and investigation of nascent DNA levels revealed that DHX9 is associated with origins of replication and that its suppression leads to a reduction of DNA replication. Our results demonstrate an essential role of DHX9 in DNA replication and normal cell cycle progression.

Indexed as

beta-GalactosidaseCell Cycle CheckpointsCellular SenescenceDEAD-box RNA HelicasesDiploidyDNA ReplicationFibroblastsHEK293 CellsHumansNeoplasm ProteinsSignal TransductionTumor Suppressor Protein p53beta-GalactosidaseDEAD-box RNA HelicasesDHX9 protein, humanNeoplasm ProteinsTP53 protein, humanTumor Suppressor Protein p53Cell CycleCell GrowthDNA ReplicationHelicasep53Senescence

Identifiers

PMID24990949
PMCPMC4132785
OpenAlexW2092850906

What OpenQuestion holds

Textmetadata
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.