Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGF beta receptor for degradation.
By Peter Kavsak, R. Rasmussen, Carrie G. Causing, S. Bonni, Hai-qing Zhu, G. Thomsen, Jeffrey L. Wrana. Molecules and Cells, 2000
1,441 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9cfdddd94220001958b7a395dc1f79c056bca975
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Citations in the corpus
- Smad transcription factors. (2005, background): “5; Kavsak et al. 2000; Suzuki et al. 2002).”
- Extracellular regulation of BMP signaling in vertebrates: a cocktail of modulators. (2002, background): “This family of enzymes, which contains HECT catalytic domains characteristic of E3-ubiquitin ligases, modulate TGF- signaling by selectively targeting the activated type I receptors (Kavsak et al., 2000; Ebisawa et al., 2001) and Smad proteins (Lo and Massagué 1999; Lin et al.”
- TGF-β Activation and Function in Immunity (2013, background): “Kavsak P, Rasmussen RK, Causing CG, Bonni S, Zhu HT, et al. Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGFβ receptor for degradation.”
- Clathrin- and non-clathrin-mediated endocytic regulation of cell signalling (2005, background): “pl?Q9HAU4">SMURF2 , which direct the ubiquitylation and subsequent degradation of the TGFβR–SMAD7 comple”
- Physiological functions of the HECT family of ubiquitin ligases (2009, background): “It has been suggested that SMURF2 targets SMAD1, SMAD2, SMAD7 and the TGFβ receptor itsel”
- Diverse Roles of TGF-β/Smads in Renal Fibrosis and Inflammation (2011, background): “In chronic kidney diseases, TGF-β1 and angiotensin II are able to induce Smad7 mRNA expression and also activate the Smurfs and arkadia-dependent ubiquitin–proteasome pathways that, in turn, degrade Smad7 protein via a post-transcriptional modification mechanism [7, 8, 37, 68, 69].”