Mechanisms of TGF-beta signaling from cell membrane to the nucleus.

By Yigong Shi, J. Massagué. Cell, 2003

3,063 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/3392550efc00b20e65731d6389b0232b807b3283

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Citations in the corpus

Dorsal-ventral patterning and neural induction in Xenopus embryos. (2004, background): “Smads 1/5/8 transduce signals of the BMP serine/threonine kinase receptors through phosphorylation of carboxy-terminal SXS sequences, thus triggering nuclear translocation (Shi & Massagué 2003).”
Transforming Growth Factor (TGF)-β signaling in cardiac remodeling (2010, unknown): “proteins [13]; Smad2 and Smad3 are activated through phosphorylation by ALK5, whereas Smad1, Smad5 and Smad8 are activated by”
TGFβ in Cancer (2008, background): “…are clustered in one family branch, and bone morphogenetic proteins (BMPs), anti-muellerian hormone (AMH, also known as MIS), and various growth and differentiation factors (GDFs) are grouped into the other branch (Derynck and Akhurst, 2007; Roberts and Wakefield, 2003; Shi and Massagué, 2003).”
RTK and TGF-β signaling pathways genes in the sea urchin genome (2006, background): “The TGF-β superfamily, which comprises 45members in humans, includes a large variety of cytokines with pleiotropic functions (Shi and Massague, 2003).”
Aberrant repair and fibrosis development in skeletal muscle (2011, background): “However, TGFb has also been shown to signal via several additional pathways, including p38 mitogen-activated protein kinase (MAPK), which requires the heparin sulfate-containing proteoglycan (HSPG) betaglycan; the Ras/MAPK kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway, which requi”
The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “Once activated the Smad2/3 form heterocomplexes with SMAD4 and translocation occurs into the nucleus where they regulate the cell type‐specific the expression of TGF‐β‐responsive genes (Miura et al., 2000; Moustakas & Heldin, 2005; Shi & Massagué, 2003).”
The logic of TGFβ signaling (2006, background): “pSer serves as a docking site for Smad4 [18,19], which is not a receptor substrate but an essential component of the resulting transcriptional complexes [20,21].”
Protection from obesity and diabetes by blockade of TGF-β/Smad3 signaling (2011, background): “TGF-b and its related factors control the development, growth, and function of diverse cell types (Shi and Massagué, 2003).”
The role of TGF-β Signaling in Myocardial Infarction and Cardiac Remodeling (2007, background): “Phosphorylation of the TβRI activates the type I receptor kinase domain, which then propagates downstream intracellular signals, through the Smad proteins, essential components in the signaling pathway of TGF-β [11] (Figure 1).”
Smad3 as a mediator of the fibrotic response (2004, background): “This domain in R-Smads interacts with the Type I receptor, contains the SSXS phosphorylation site and mediates formation of R-Smad/Smad4 oligomers.”