Evidence map›Paper›PMID 31860636›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2019

The Oncogene PIM1 Contributes to Cellular Senescence by Phosphorylating Staphylococcal Nuclease Domain-Containing Protein 1 (SND1).

Wu Wu, Aiqing Yu, Keyu Chen, Peilin Lu, Jianming Yang, Kun Liu, Zebin Mao, Zhi Yao

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 1 country.

Wu WuDepartment of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China (mainland).
Aiqing YuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China (mainland).
Keyu ChenDepartment of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China (mainland).
Peilin LuDepartment of Dermatology, Sichuan Provincial Fourth People's Hospital, Chengdu, Sichuan, China (mainland).
Jianming YangDepartment of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China (mainland).
Kun LiuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China (mainland).
Zebin MaoKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China (mainland).
Zhi YaoDepartment of Immunology, School of Basic Medical Science, Tianjin Medical University, Tianjin, China (mainland).
Tianjin Medical University · CNPeking University · CNFourth People's Hospital of Sichuan Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

<strong>BACKGROUND</strong> The oncogene PIM1, encoding a constitutively active serine/threonine protein kinase, is involved in the regulation of cell proliferation, survival, differentiation, and apoptosis. There is a growing body of literature on the role of PIM1-mediated cellular senescence, but the precise mechanism remains unclear. <strong>MATERIAL AND METHODS</strong> Silver staining and LC-MS/MS analysis were performed to investigate the protein interacting with PIM1. Immunofluorescence, Co-IP, and Western blot assay were used to assess the interaction of PIM1 and SND1. EdU incorporation and CCK8 assay were used to detect cell proliferation and immunohistochemistry was used to detect the level of the indicated protein. <strong>RESULTS</strong> We found that PIM1 can bind directly and phosphorylate SND1. In addition, decreased expression of SND1 leads to the upregulation of SASP. SND1 is involved in cellular senescence induced by PIM1. <strong>CONCLUSIONS</strong> We investigated the role of PIM1 in oncogene-induced normal cellular senescence. Our results promote further understanding of the mechanisms underlying OIS and suggest potential applications for preventing tumorigenesis.

Indexed as

ApoptosisCell DifferentiationCell Line, TumorCell ProliferationCellular SenescenceChromatography, LiquidEndonucleasesHEK293 CellsHumansNuclear ProteinsPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene Proteins c-pim-1Tandem Mass SpectrometryEndonucleasesNuclear ProteinsPIM1 protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-pim-1SND1 protein, human

Identifiers

PMID31860636
PMCPMC6876065
OpenAlexW2988935829

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.