Controlling TGF-beta signaling.
By J. Massagué, Y. G. Chen. Genes & Development, 2000
835 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/b75edc91314331539f8038d82ab3405fecb88e31
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- D. Montani
- M. Humbert
- S. Günther
- G. Simonneau
- P. Dorfmüller
- S. Scollen
- O. Sitbon
- F. Perros
Citations in the corpus
- The logic of TGFβ signaling (2006, unknown): “powerful signaling process (for reviews see [29,30]).”
- TGF-β signalling pathway and breast cancer susceptibility (2011, background): “SMAD6 and SMAD7 block phosphorylation of SMAD2 or SMAD3 and act as inhibitors of the TGF-b signaling pathway (15, 32).”
- Exosomes Derived from Human Umbilical Cord Mesenchymal Stem Cells Alleviate Liver Fibrosis (2013, background): “Some studies have reported that upon phosphorylation, Smad2 and Smad3 form complexes with Smad4 and, subsequently, translocate into the nucleus to regulate the transcription of target genes responsible for EMT, such as Smad7, snail, and collagen type I [8,34,35].”
- Pulmonary arterial hypertension (2013, background): “bound type I receptors initiating phosphorylation of the type I receptor.(5) This pathway seems to be critical in”
- TGFβ in Cancer (2008, background): “A structurally diverse group of proteins (ligand traps) that “trap” TGFβ family members to limit their access to membrane receptors play critical roles during morphogenesis of the embryo and in the adult (De Robertis and Kuroda, 2004; Massagué and Chen, 2000).”