Signal Transduction by the TGF-β Superfamily
By L. Attisano, Jeffrey L. Wrana. Science, 2002
1,194 citations recorded by the source corpus.
Subfields: Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/b94f69c7668a67a31b18f500fda069caec8ab605
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
In Pathology and Forensic Medicine
Citations in the corpus
- Smad transcription factors. (2005, methodology): “For more information on the biology of the TGF family, we would recommend several classical reviews (Letterio and Roberts 1998; Whitman 1998; Massagué and Chen 2000; Massagué et al. 2000; Derynck et al. 2001; Attisano and Wrana 2002; Schier 2003).”
- The basics of epithelial–mesenchymal transition (EMT): A study from a structure, dynamics, and functional perspective (2019, background): “TGFβ regulates transcription by Smad‐dependent and independent TGFβ receptor signaling pathways (Attisano & Wrana, 2002; Long, Zuo, & Park, 2005; Van Grunsven et al., 2007).”
- TGF-β/Smad signaling in renal fibrosis (2015, background): “Additionally, TGF-β1 is able to function through the Smad-independent pathways, including p38, ERK (Extracellular-signal-regulated kinase), MAPK, RhoGTPases, Rac, Cdc42, ILK (Integrin linked kinase) (Attisano and Wrana, 2002; Derynck and Zhang, 2003; Li et al., 2009; Loeffler andWolf, 2014).”
- TGF‐β activates Erk MAP kinase signalling through direct phosphorylation of ShcA (2007, background): “TGF-b proteins are key regulators of development and tissue differentiation (Attisano and Wrana, 2002), and signal through complexes of type II (TbRII) and type I (TbRI) receptors that are characterised as serine-threonine kinases (Chen et al, 1995).”
- TGF-β1-induced Migration of Bone Mesenchymal Stem Cells Couples Bone Resorption and Formation (2009, background): “It is well established that phosphorylation of receptor-regulated SMADs (R-SMADs) by TβRI is the primary TGF-β signaling pathwa”
- Diverse cellular and molecular mechanisms contribute to epithelial plasticity and metastasis (2003, background): “Cooperation between TGF-β receptors and RTKs or other receptors involves many mechanisms (see Ref”
- A Small Molecule Inhibitor of Tgf-β Signaling Replaces Sox2 in Reprogramming by Inducing Nanog (2009, methodology): “We have used a phenotypic chemical screen to identify compounds that can replace the reprogramming transcription factor Sox2 and have confirmed the mechanism by which the most potent compound acts: RepSox replaces Sox2 by inhibiting the broadly expressed Tgf-b signaling pathway (Attisano and Wrana, ”
- Preventing or reducing late side effects of radiation therapy: radiobiology meets molecular pathology (2006, background): “The signalling pathway itself is rather simple: the only established intracellular signalling effectors are the Smad proteins, of which there are five R-Smads (receptor-regulated Smads; SMAD1 , 2, 3, 5 and 8) that are directly phosphorylated by the type I receptor, a co-Smad ( SMAD4 ) that forms he”