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Perspectives
GDF3 at the Crossroads of TGF-beta Signaling
Ariel J. Levine and Ali H. Brivanlou
volume 5 | issue 10
15 may 2006Pages: 1069 - 1073
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Embryonic stem (ES) cells present an excellent system for addressing the relevance of our current knowledge about how cell fate is determined and how cells integrate multiple signals into a single outcome as a function of time. Many of the factors that mediate these phenomena have been discovered through classical embryological experiments and are organized into several major signal transduction pathways including TGF-β/BMP, Jak-STAT, Hedgehog, Wnt, Notch and FGF/MAPK.1 This review will summarize the current understanding of TGF-β signaling in ES and focus on early embryological roles of the TGF-β member, GDF-3. GDF-3 is associated with the undifferentiated state of ES cells and two recent and contradictory reports examined the function and mechanism of GDF-3 in the context of both stem cells and early embryonic differentiations. While Levine and Brivanlou found that GDF-3 inhibits its own subfamily members (the BMPs), Chen and colleagues found that GDF-3 acts as a nodal-like TGF-β ligand. These combined findings raise the intriguing possibility that GDF-3 acts as a bi-functional protein, to regulate the balance between the two modes of TGF-β signaling.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.