ArticleMolecular and cellular biology2005
Oct-3/4 maintains the proliferative embryonic stem cell state via specific binding to a variant octamer sequence in the regulatory region of the UTF1 locus.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 99 citations in OpenAlex.
- Cell-type-specific functionality encoded within the intrinsically disordered regions of OCT4.Nature communications · 2025Article
- UTF1 Expression is Important for the Generation and Maintenance of Human iPSCs.Stem cell reviews and reports · 2025Article
- Expression and clinical significance of undifferentiated embryonic cell transcription factor 1 in breast cancer.Translational cancer research · 2023Article
- Evolutionary origin of vertebrate OCT4/POU5 functions in supporting pluripotency.Nature communications · 2022Article
- Key features of the POU transcription factor Oct4 from an evolutionary perspective.Cellular and molecular life sciences : CMLS · 2021Review
- An Insight into the Role of UTF1 in Development, Stem Cells, and Cancer.Stem cell reviews and reports · 2021Review
- Directed Evolution of an Enhanced POU Reprogramming Factor for Cell Fate Engineering.Molecular biology and evolution · 2021Article
- Biological importance of OCT transcription factors in reprogramming and development.Experimental & molecular medicine · 2021Review
- Article
- Pluripotency reprogramming by competent and incompetent POU factors uncovers temporal dependency for Oct4 and Sox2.Nature communications · 2019Article
- Identifying and targeting cancer stem cells in leiomyosarcoma: prognostic impact and role to overcome secondary resistance to PI3K/mTOR inhibition.Journal of hematology & oncology · 2019Article
- Diversity among POU transcription factors in chromatin recognition and cell fate reprogramming.Cellular and molecular life sciences : CMLS · 2018Review
- Embryonic lethality and defective male germ cell development in mice lacking UTF1.Scientific reports · 2017Article
- Article
- Quantitative profiling of selective Sox/POU pairing on hundreds of sequences in parallel by Coop-seq.Nucleic acids research · 2017Article
- Cooperative DNA Recognition Modulated by an Interplay between Protein-Protein Interactions and DNA-Mediated Allostery.PLoS computational biology · 2015Article
- Expression profile of undifferentiated cell transcription factor 1 in normal and cancerous human epithelia.International journal of experimental pathology · 2014Article
- Article
- Review
- Use of UTF1 genetic control elements as iPSC reporter.Stem cell reviews and reports · 2013Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The POU transcription factor Oct-3/4 has been shown to be critical for maintaining embryonic stem (ES) cell character. However, the molecular mechanisms underlying its function remain elusive. We have previously shown that among the POU transcription factor family of proteins, Oct-3/4 alone is able to bind to the regulatory region of the UTF1 gene bearing a variant octamer sequence together with Sox-2. Here, we demonstrate using Oct-3/4-Oct-6 chimeras that there is a precise correlation between the ability of proteins to form a complex on the UTF1 enhancer with Sox-2 and the ability to maintain the stem cell state in ES cells. Different chimeric proteins show differential abilities to form a Sox-2-containing complex on the UTF1 regulatory region, with a decrease in efficiency of the complex formation accompanied by a decrease in the level of UTF1 expression and the rate of cell proliferation. Overexpression of UTF1 in these slow-growing cells was able to restore their proliferation rate to wild-type levels. Moreover, UTF1 was also observed to have an effect on teratoma formation. These results suggest a molecular pathway by which Oct-3/4 induces rapid proliferation and tumorigenic properties of ES cells through activation of the UTF1 gene.
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