Abstract
The cytokine LIF and its downstream effector STAT3 are essential for maintenance of pluripotency in mouse ES cells. The requirement for the transcription factor Oct3/4 for ES cell pluripotency is also welldocumented. However, LIF is not involved in self-renewal of human ES cells, suggesting that other pathways must play an important role in this process. The importance of other signal transduction pathways, including BMP and Wnt signalings, as well as novel transcription factors such as Nanog, is now being recognized. We will review the rapid progress that has been made in identifying and dissecting the intracellular signaling pathways that contribute to self-renewal of pluripotent mouse and human ES cells.
Keywords: Growth factor, Cytokine, Regenerative medicine, Transcription factor, Crosstalk
Current Stem Cell Research & Therapy
Title: Intracellular Signaling Pathways Regulating Pluripotency of Embryonic Stem Cells
Volume: 1 Issue: 1
Author(s): Keisuke Okita and Shinya Yamanaka
Affiliation:
Keywords: Growth factor, Cytokine, Regenerative medicine, Transcription factor, Crosstalk
Abstract: The cytokine LIF and its downstream effector STAT3 are essential for maintenance of pluripotency in mouse ES cells. The requirement for the transcription factor Oct3/4 for ES cell pluripotency is also welldocumented. However, LIF is not involved in self-renewal of human ES cells, suggesting that other pathways must play an important role in this process. The importance of other signal transduction pathways, including BMP and Wnt signalings, as well as novel transcription factors such as Nanog, is now being recognized. We will review the rapid progress that has been made in identifying and dissecting the intracellular signaling pathways that contribute to self-renewal of pluripotent mouse and human ES cells.
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Cite this article as:
Okita Keisuke and Yamanaka Shinya, Intracellular Signaling Pathways Regulating Pluripotency of Embryonic Stem Cells, Current Stem Cell Research & Therapy 2006; 1 (1) . https://dx.doi.org/10.2174/157488806775269061
DOI https://dx.doi.org/10.2174/157488806775269061 |
Print ISSN 1574-888X |
Publisher Name Bentham Science Publisher |
Online ISSN 2212-3946 |
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