IGF antagonizes the Wnt/β-Catenin pathway and promotes differentiation of extra-embryonic endoderm
Mouse F9 teratocarcinoma cells are an established model for the differentiation of extra-embryonic endoderm (ExEn). Primitive endoderm, parietal and visceral endoderm can be generated by stimulation of F9 cells with retinoic acid and dibutyryl cyclic adenosine monophosphate. Here we show that Wnt/β-...
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| Hauptverfasser: | , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
5 October 2014
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| In: |
Differentiation
Year: 2014, Jahrgang: 87, Heft: 5, Pages: 209-219 |
| ISSN: | 1432-0436 |
| DOI: | 10.1016/j.diff.2014.07.003 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.diff.2014.07.003 Verlag, lizenzpflichtig, Volltext: http://www.sciencedirect.com/science/article/pii/S0301468114000498 
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| Verfasserangaben: | Judith Schlupf, Herbert Steinbeisser |
| Zusammenfassung: | Mouse F9 teratocarcinoma cells are an established model for the differentiation of extra-embryonic endoderm (ExEn). Primitive endoderm, parietal and visceral endoderm can be generated by stimulation of F9 cells with retinoic acid and dibutyryl cyclic adenosine monophosphate. Here we show that Wnt/β-Catenin signaling is down-regulated during ExEn differentiation in F9 cells and that the inhibition of the Wnt pathway promotes differentiation of the three extra-embryonic endoderm lineages. Wnt inhibition is achieved through the IGF pathway, which is up-regulated during differentiation. IGF signaling antagonizes the Wnt pathway by stimulating transcription of axin2 and by stabilizing Axin1 protein. Both Axin1 and Axin2 are components of the β-Catenin destruction complex and act as intra-cellular inhibitors of the Wnt/β-Catenin pathway. The data presented reveal a mechanism which restricts pluripotency of undifferentiated cells and directs them toward extra-embryonic lineages. |
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| Beschreibung: | Gesehen am 13.08.2020 |
| Beschreibung: | Online Resource |
| ISSN: | 1432-0436 |
| DOI: | 10.1016/j.diff.2014.07.003 |