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          Institute: MPI für molekulare Biomedizin     Collection: Jahrbuch 2017 (publ. 2016, arch)     Display Documents



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ID: 732124.0, MPI für molekulare Biomedizin / Jahrbuch 2017 (publ. 2016, arch)
Enhanced OCT4 transcriptional activity substitutes for exogenous SOX2 in cellular reprogramming
Authors:Marthaler, A. G.; Adachi, K.; Tiemann, U.; Wu, G.; Sabour, D.; Velychko, S.; Kleiter, I.; Scholer, H. R.; Tapia, N.
Date of Publication (YYYY-MM-DD):2016
Title of Journal:Sci Rep
Volume:6
Start Page:19415
Review Status:Internal review
Audience:Not Specified
Abstract / Description:Adenoviral early region 1A (E1A) is a viral gene that can promote cellular proliferation and de-differentiation in mammalian cells, features required for the reprogramming of somatic cells to a pluripotent state. E1A has been shown to interact with OCT4, and as a consequence, to increase OCT4 transcriptional activity. Indeed, E1A and OCT4 are sufficient to revert neuroepithelial hybrids to pluripotency, as demonstrated in previous cell fusion experiments. However, the role that E1A might play in the generation of induced pluripotent stem cells (iPSCs) has not been investigated yet. In this report, we show that E1A can generate iPSCs in combination with OCT4 and KLF4, thus replacing exogenous SOX2. The generated iPSCs are bona fide pluripotent cells as shown by in vitro and in vivo tests. Overall, our study suggests that E1A might replace SOX2 through enhancing OCT4 transcriptional activity at the early stages of reprogramming.
External Publication Status:published
Document Type:Article
Communicated by:Jeanine Müller-Keuker
Affiliations:MPI für molekulare Biomedizin
External Affiliations:Medical Faculty, Heinrich Heine University, Moorenstrasse 5, 40225 Dusseldorf, Germany. Department of Neurology, St Josef Hospital, Ruhr University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany. Medical Faculty, University of Munster, Domagkstrasse 3, 48149 Munster, Germany.
Identifiers:ISSN:2045-2322 (Electronic) 2045-2322 (Linking) %R 10.1... [ID No:1]
URL:http://www.ncbi.nlm.nih.gov/pubmed/26762895 [ID No:2]
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