The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Multiple targets of miR-302 and miR-372 promote reprogramming of human fibroblasts to induced pluripotent stem cells
Open accessAbstract
The embryonic stem cell–specific cell cycle–regulating (ESCC) family of microRNAs (miRNAs) enhances reprogramming of mouse embryonic fibroblasts to induced pluripotent stem cells. Here we show that the human ESCC miRNA orthologs hsa-miR-302b and hsa-miR-372 promote human somatic cell reprogramming. Furthermore, these miRNAs repress multiple target genes, with downregulation of individual targets only partially recapitulating the total miRNA effects. These targets regulate various cellular processes, including cell cycle, epithelial-mesenchymal transition (EMT), epigenetic regulation and vesicular transport. ESCC miRNAs have a known role in regulating the unique embryonic stem cell cycle. We show that they also increase the kinetics of mesenchymal-epithelial transition during reprogramming and block TGFβ-induced EMT of human epithelial cells. These results demonstrate that the ESCC miRNAs promote dedifferentiation by acting on multiple downstream pathways. We propose that individual miRNAs generally act through numerous pathways that synergize to regulate and enforce cell fate decisions.
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Cites
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Cited by
Molecular mechanisms of epithelial–mesenchymal transition
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Self-citationTGF-β signaling and epithelial–mesenchymal transition in cancer progression
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Self-citationSignaling Receptors for TGF-β Family Members
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Nanog, Pou5f1 and SoxB1 activate zygotic gene expression during the maternal-to-zygotic transition
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Metadata
- Authors
- Subramanyam, D., Lamouille, S., Judson, R. L., Liu, J. Y., Bucay, N., Derynck, R., & Blelloch, R.
- Venue
- Nature Biotechnology
- Published
- 2011-04-13
- Volume
- 29
- Issue
- 5
- Pages
- 443-448
- ISSN
- 0733-222X (ISSN-L)
- 1087-0156
- 1546-1696
- OpenAlex
- W1999389272
- Cited by
- 598
- References
- 38
- FWCI
- 27.74
- Type
- journal article
- Language
- en
- Open access
- green
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