Furthermore, classical activin signaling via Smadproteins is necessary for this synergy.
2
The Ski family of nuclear oncoproteins represses TGF-beta signaling through interactions with the Smadproteins.
3
This repression is transmitted through TGF-beta signaling and can be regulated by other Smadproteins.
4
Smadproteins have been identified as major components in the intracellular signaling of TGF-beta family members.
5
Once in the nucleus Smadproteins interact with other DNA binding proteins to regulate transcription of specific target genes.
6
Genetic studies of Dpp signaling led to the identification of Smadproteins as central mediators of signal transduction by TGF-beta family members.
7
Changes in Smadproteins and their complexes upon treatment with TGF-beta were studied in mink lung epithelial (Mv1Lu) cell cultures.
8
Smadproteins are substrates of the TGF-beta type I receptor and are responsible for transducing receptor signals to target genes in the nucleus.
9
Transduction of TGF-beta signaling depends on the phosphorylation and activation of Smadproteins by heteromeric complexes of ligand-specific type I and II receptors.
10
We show that Cyr61 transcription is activated by TGFbeta and that the human Cyr61 promoter contains consensus sequences that bind Smadproteins.