Evidence map›Paper›PMID 25515777›Full record

ArticleScientific reports2014

The dosage of Patz1 modulates reprogramming process.

Hui Ma, Jin Rong Ow, Bobby Cheng Peow Tan, Ziyi Goh, Bo Feng, Yuin Han Loh, Monica Fedele, Hu Li, Qiang Wu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

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  13. Structural analysis of the PATZ1 BTB domain homodimer.Acta crystallographica. Section D, Structural biology · 2020
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Divergent modulation of normal and neoplastic stem cells by thrombospondin-1 and CD47 signaling.The international journal of biochemistry & cell biology · 2016
    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

9 authors at 6 institutions in 4 countries.

Hui MaDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, MD6, Centre for Translational Medicine, Level 14, South Core, 14 Medical Drive Singapore 117597.
Jin Rong OwDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, MD6, Centre for Translational Medicine, Level 14, South Core, 14 Medical Drive Singapore 117597.
Bobby Cheng Peow TanGenome Institute of Singapore, 60 Biopolis Street, Singapore 138672.
Ziyi GohDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, MD6, Centre for Translational Medicine, Level 14, South Core, 14 Medical Drive Singapore 117597.
Bo FengSchool of Biomedical Sciences, the Chinese University of Hong Kong, Lo Kwee-Seong Integrated Biomedical Sciences Building, Shatin, NT, Hong Kong.
Yuin Han LohInstitute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore 138673.
Monica FedeleInstitute of Experimental Endocrinology and Oncology, CNR, 80131 Naples, Italy.
Hu LiCenter for Individualized Medicine, Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.
Qiang WuDepartment of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, MD6, Centre for Translational Medicine, Level 14, South Core, 14 Medical Drive Singapore 117597.
National University of Singapore · SGChinese University of Hong Kong · CNGenome Institute of Singapore · SGInstitute for Experimental Endocrinology and Oncology · ITInstitute of Molecular and Cell Biology · SGMayo Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The acquisition of pluripotent cells can be achieved by combined overexpression of transcription factors Oct4, Klf4, Sox2 and c-Myc in somatic cells. This cellular reprogramming process overcomes various barriers to re-activate pluripotency genes and re-acquire the highly dynamic pluripotent chromatin status. Many genetic and epigenetic factors are essentially involved in the reprogramming process. We previously reported that Patz1 is required for maintenance of ES cell identity. Here we report that Patz1 plays an inhibitory role in OKSM-induced reprogramming process since more iPS colonies can be induced from Patz1(+/-) MEFs than wild type MEFs; while the addition of Patz1 significantly repressed reprogramming efficiency. Patz1(+/-) MEFs can surpass the senescence barrier of Ink4a/Arf locus, thus enhancing iPS colonies formation. Moreover, Patz1(+/-) MEFs displayed higher levels of acetylated histone H3, H3K4me2, H3K4me3, H3K36me3 and lower levels of histone H3K9me3 and HP1α, indicating that heterozygous knockout of Patz1 results in a globally open chromatin which is more accessible for transcriptional activation. However, Patz1(-/-) MEFs gave the lowest reprogramming efficiency which may result from cell senescence trigged by up-regulated Ink4a/Arf locus. Together, we have demonstrated that the dosage of Patz1 modulates reprogramming process via significantly influencing cell senescence, proliferation and chromatin structure.

Indexed as

AnimalsCell LineCellular ReprogrammingCellular SenescenceChromatinCyclin-Dependent Kinase Inhibitor p16Embryonic Stem CellsFibroblastsHistonesKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicePluripotent Stem CellsTranscriptional ActivationChromatinCyclin-Dependent Kinase Inhibitor p16HistonesKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription Factors

Identifiers

PMID25515777
PMCPMC4268633
OpenAlexW1986566442

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.