Evidence map›Paper›PMID 25611385›Full record

ArticleCell death & disease2015

A G-quadruplex DNA structure resolvase, RHAU, is essential for spermatogonia differentiation.

X Gao, W Ma, J Nie, C Zhang, J Zhang, G Yao, J Han, J Xu, B Hu, Y Du and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 42 citations in OpenAlex.

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  19. Single-molecule imaging reveals a common mechanism shared by G-quadruplex-resolving helicases.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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

14 authors at 6 institutions in 1 country.

X GaoMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
W MaShanghai Key Laboratory for Molecular Andrology, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Shanghai 200031, China.
J NieMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
C ZhangShanghai Key Laboratory for Molecular Andrology, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Shanghai 200031, China.
J ZhangMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
G YaoShanghai Key Laboratory for Molecular Andrology, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Shanghai 200031, China.
J HanMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
J XuMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
B HuMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Y DuMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Q ShiHefei National Laboratory for Physical Sciences at Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, 230026 Anhui, China.
Z YangMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
X HuangMOE Key Laboratory of Model Animal for Disease Study, Nanjing Biomedical Research Institute, National Resource Center for Mutant Mice, Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Y Zhang1] Shanghai Key Laboratory for Molecular Andrology, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Shanghai 200031, China [2] Shanghai Institute of Planned Parenthood Research, Shanghai 200032, China.
Model Animal Research Center · CNNanjing University · CNShanghai Institutes for Biological Sciences · CNCenter for Excellence in Molecular Cell Science · CNHefei National Center for Physical Sciences at Nanoscale · CNShanghai Institute of Planned Parenthood Research · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

G-quadruplex (G4) DNA and G4 DNA resolvase are involved in a variety of biological processes. To understand the biological function of G4 DNA structures and their resolvases in spermatogenesis, we investigated the distribution of G4 structures in mouse testis and identified their alterations during spermatogenesis. Meanwhile, we studied the function of RNA helicase associated with AU-rich element (RHAU), a G4 DNA resolvase, in spermatogenesis with a germ-cell-specific knockout mouse model. The results showed that the ablation of RHAU in germ cells caused the increase of G4 structures and thus resulted in the decrease of spermatogonial differentiation. c-kit, a spermatogonia differentiation-related gene, contains two G4 DNA motifs on its promoter. We found its expression was significantly downregulated in RHAU conditional knockout testis. A further analysis demonstrated that RHAU directly bound to the G4 structures to activate c-kit expression. We concluded that RHAU regulates spermatogonia differentiation by promoting c-kit expression via directly binding to the G4 DNA motifs c-kit promoter.

Indexed as

Cell DifferentiationG-QuadruplexesAdenosine TriphosphateAnimalsApoptosisAzoospermiaBase SequenceCell ProliferationDEAD-box RNA HelicasesDNAGene DeletionGene Expression RegulationMaleMeiosisMiceMice, KnockoutAdenosine TriphosphateDEAD-box RNA HelicasesDhx36 protein, mouseDNAProto-Oncogene Proteins c-kitRecombinases

Identifiers

PMID25611385
PMCPMC4669769
OpenAlexW1966934059

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.