Evidence map›Paper›PMID 25627688›Full record

ArticleThe Journal of biological chemistry2015

Tudor staphylococcal nuclease (Tudor-SN), a novel regulator facilitating G1/S phase transition, acting as a co-activator of E2F-1 in cell cycle regulation.

Chao Su, Chunyan Zhang, Adiam Tecle, Xue Fu, Jinyan He, Juan Song, Wei Zhang, Xiaoming Sun, Yuanyuan Ren, Olli Silvennoinen and 4 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 94 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

14 authors at 5 institutions in 3 countries.

Chao SuFrom the Departments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Immunology, School of Basic Medical Sciences, Laboratory of Molecular Immunology, Research Center of Basic Medical Science, and the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Chunyan ZhangFrom the Departments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Immunology, School of Basic Medical Sciences, Laboratory of Molecular Immunology, Research Center of Basic Medical Science, and the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Adiam TecleImmunology, School of Basic Medical Sciences, Laboratory of Molecular Immunology, Research Center of Basic Medical Science, and the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Xue FuFrom the Departments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Immunology, School of Basic Medical Sciences, Laboratory of Molecular Immunology, Research Center of Basic Medical Science, and the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Jinyan Hethe Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Juan SongFrom the Departments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Immunology, School of Basic Medical Sciences, Laboratory of Molecular Immunology, Research Center of Basic Medical Science, and the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Wei ZhangFrom the Departments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Xiaoming SunFrom the Departments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Yuanyuan RenFrom the Departments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Olli Silvennoinenthe Institute of Medical Technology, University of Tampere, Tampere University Hospital, Biokatu 8, FI-33014 Tampere, Finland, and.
Zhi YaoImmunology, School of Basic Medical Sciences, the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China.
Xi Yangthe Department of Immunology, University of Manitoba, Winnipeg R3E 0T5, Canada.
Minxin Weithe Department of Cardiovascular Surgery, Tianjin Medical University General Hospital, Tianjin 300070, China minxinw@126.com.
Jie YangFrom the Departments of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Immunology, School of Basic Medical Sciences, Laboratory of Molecular Immunology, Research Center of Basic Medical Science, and the Tianjin Key Laboratory of Cellular and Molecular Immunology, Tianjin Medical University, Tianjin, 300070, China, the Key Laboratory of Educational Ministry of China, Tianjin Medical University, Tianjin, 300070, China, the Institute of Medical Technology, University of Tampere, Tampere University Hospital, Biokatu 8, FI-33014 Tampere, Finland, and yangj@tijmu.edu.cn.
Tianjin Medical University · CNTampere University · FITampere University Hospital · FITianjin Medical University General Hospital · CNUniversity of Manitoba · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tudor staphylococcal nuclease (Tudor-SN) is a multifunctional protein implicated in a variety of cellular processes. In the present study, we identified Tudor-SN as a novel regulator in cell cycle. Tudor-SN was abundant in proliferating cells whereas barely expressed in terminally differentiated cells. Functional analysis indicated that ectopic overexpression of Tudor-SN promoted the G1/S transition, whereas knockdown of Tudor-SN caused G1 arrest. Moreover, the live-cell time-lapse experiment demonstrated that the cell cycle of MEF(-/-) (knock-out of Tudor-SN in mouse embryonic fibroblasts) was prolonged compared with wild-type MEF(+/+). We noticed that Tudor-SN was constantly expressed in every cell cycle phase, but was highly phosphorylated in the G1/S border. Further study revealed that Tudor-SN was a potential substrate of Cdk2/4/6, supportively, we found the physical interaction of endogenous Tudor-SN with Cdk4/6 in G1 and the G1/S border, and with Cdk2 in the G1/S border and S phase. In addition, roscovitine (Cdk1/2/5 inhibitor) or CINK4 (Cdk4/6 inhibitor) could inhibit the phosphorylation of Tudor-SN, whereas ectopic overexpression of Cdk2/4/6 increased the Tudor-SN phosphorylation. The underlying molecular mechanisms indicated that Tudor-SN could physically interact with E2F-1 in vivo, and could enhance the physical association of E2F-1 with GCN5 (a cofactor of E2F-1, which possesses histone acetyltransferase activity), and promote the binding ability of E2F-1 to the promoter region of its target genes CYCLIN A and E2F-1, and as a result, facilitate the gene transcriptional activation. Taken together, Tudor-SN is identified as a novel co-activator of E2F-1, which could facilitate E2F-1-mediated gene transcriptional activation of target genes, which play essential roles in G1/S transition.

Indexed as

G1 PhaseS PhaseAmino Acid SequenceAnimalsCell Cycle CheckpointsCells, CulturedCyclin-Dependent KinasesCyclinsE2F1 Transcription FactorEndonucleasesGene Knockdown TechniquesHeLa CellsHumansMiceMice, Inbred BALB CMice, Inbred C57BLCyclin-Dependent KinasesCyclinsE2F1 protein, humanE2f1 protein, mouseE2F1 Transcription FactorEndonucleasesNuclear ProteinsSND1 protein, humanSnd1 protein, mouseCell CycleCyclin-dependent Kinase (CDK)E2F-1G1/S TransitionGene TranscriptionProtein PhosphorylationTranscription CoactivatorTranscription RegulationTudor-SN

Identifiers

PMID25627688
PMCPMC4358140
OpenAlexW2027521216

What OpenQuestion holds

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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.