ArticleStem cell reports2014
Counteracting activities of OCT4 and KLF4 during reprogramming to pluripotency.
Article in Stem cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Sin3a drives mesenchymal-to-epithelial transition through cooperating with Tet1 in somatic cell reprogramming.Stem cell research & therapy · 2022Article
- A genomic atlas of human adrenal and gonad development.Wellcome open research · 2017Article
- The SIN3A/HDAC Corepressor Complex Functionally Cooperates with NANOG to Promote Pluripotency.Cell reports · 2017Article
- Enhanced OCT4 transcriptional activity substitutes for exogenous SOX2 in cellular reprogramming.Scientific reports · 2016Article
- Epigenetic Aberrations Are Not Specific to Transcription Factor-Mediated Reprogramming.Stem cell reports · 2016Article
- Dissecting the role of distinct OCT4-SOX2 heterodimer configurations in pluripotency.Scientific reports · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differentiated cells can be reprogrammed into induced pluripotent stem cells (iPSCs) after overexpressing four transcription factors, of which Oct4 is essential. To elucidate the role of Oct4 during reprogramming, we investigated the immediate transcriptional response to inducible Oct4 overexpression in various somatic murine cell types using microarray analysis. By downregulating somatic-specific genes, Oct4 induction influenced each transcriptional program in a unique manner. A significant upregulation of pluripotent markers could not be detected. Therefore, OCT4 facilitates reprogramming by interfering with the somatic transcriptional network rather than by directly initiating a pluripotent gene-expression program. Finally, Oct4 overexpression upregulated the gene Mgarp in all the analyzed cell types. Strikingly, Mgarp expression decreases during the first steps of reprogramming due to a KLF4-dependent inhibition. At later stages, OCT4 counteracts the repressive activity of KLF4, thereby enhancing Mgarp expression. We show that this temporal expression pattern is crucial for the efficient generation of iPSCs.
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Registered trials
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.