Signaling cross-talk between TGF-β/BMP and other pathways
By Xing Guo, Xiao-Fan Wang. Cell Research, 2009
943 citations recorded by the source corpus.
Transforming growth factor-beta (TGF-β)/bone morphogenic protein (BMP) signaling is involved in the vast majority of cellular processes and is fundamentally important during the entire life of all metazoans. Deregulation of TGF-β/BMP activity almost invariably leads to developmental defects and/or diseases, including cancer. The proper functioning of the TGF-β/BMP pathway depends on its constitutive and extensive communication with other signaling pathways, leading to synergistic or antagonistic effects and eventually desirable biological outcomes. The nature of such signaling cross-talk is overwhelmingly complex and highly context-dependent. Here we review the different modes of cross-talk between TGF-β/BMP and the signaling pathways of Mitogen-activated protein kinase, phosphatidylinositol-3 kinase/Akt, Wnt, Hedgehog, Notch, and the interleukin/interferon-gamma/tumor necrosis factor-alpha cytokines, with an emphasis on the underlying molecular mechanisms.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/1c32a46a8a8b22fa06bf3cfedb1126fd96ccbcb9
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- R. Weinberg
- Christine L. Chaffer
- A. Richardson
- C. Scheel
- Wenjun Guo
- Ferenc Reinhardt
- M. Matzuk
- George W. Bell
Citations in the corpus
- Paracrine and autocrine signals induce and maintain mesenchymal and stem cell states in the breast (2011, background): “…was also drawn to possible modulation of TGF-b by BMP signaling: mutual antagonism of TGF-b and BMP signaling pathways at several levels has been described (Guo and Wang, 2009), and BMP signaling is known to antagonize the TGF-b-driven EMT occurring during renal fibrosis (Zeisberg et al., 2003).”
- The mammalian ovary from genesis to revelation. (2009, background): “Because there is extensive cross talk between TGF and hedgehog pathways in several cell types and tissues (263), it would be interesting to determine whether components of hedgehog signaling are altered in Gdf9 null mice, contributing to the absence of thecal differentiation as a result of GDF9 defi”