• Publications
  • Influence
Direct binding of Smad3 and Smad4 to critical TGFβ‐inducible elements in the promoter of human plasminogen activator inhibitor‐type 1 gene
The identification of Smad3/Smad4 binding sequences, termed CAGA boxes, within the promoter of the human PAI‐1 gene is reported, which suggest that this may be a widely used motif in TGFβ‐regulated transcription. Expand
Balancing the activation state of the endothelium via two distinct TGF‐β type I receptors
It is reported that TGF‐β can activate two distinct type I receptor/Smad signalling pathways with opposite effects, and the results suggest that T GF‐β regulates the activation state of the endothelium via a fine balance between ALK5 and ALK1 signalling. Expand
TGF-beta signalling from cell membrane to nucleus through SMAD proteins.
Inhibitory SMADs have been identified that block the activation of these pathway-restricted SMADS that direct transcription to effect the cell's response to TGF-beta. Expand
Identification of Smad7, a TGFbeta-inducible antagonist of TGF-beta signalling.
The identification of Smad7 is reported, which is related to Smad6 and associates stably with the TGF-beta receptor complex, but is not phosphorylated upon TGF -beta stimulation. Expand
Activin receptor-like kinase 1 modulates transforming growth factor-beta 1 signaling in the regulation of angiogenesis.
  • S. P. Oh, T. Seki, +8 authors E. Li
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences…
  • 14 March 2000
The results suggest that the balance between the ALK1 and ALK5 signaling pathways in endothelial cells plays a crucial role in determining vascular endothelial properties during angiogenesis. Expand
TGF‐β receptor‐mediated signalling through Smad2, Smad3 and Smad4
It is shown that Smad2 and Smad3 interacted with the kinase‐deficient TGF‐β type I receptor (TβR)‐I after it was phosphorylated by TβR‐II kinase, which suggests that T GF‐β induces heteromeric complexes of Smad 2, 3 and 4, and their concomitant translocation to the nucleus, which is required for efficient TGF-β signal transduction. Expand
Identification and Functional Characterization of Distinct Critically Important Bone Morphogenetic Protein-specific Response Elements in the Id1 Promoter*
It is reported that Id1, a dominant negative inhibitor of basic helix-loop-helix proteins, is a direct target gene for BMP, and the results provide important new insights into how the BMP/Smad pathway can specifically activate target genes. Expand
Activin receptor-like kinase (ALK)1 is an antagonistic mediator of lateral TGFbeta/ALK5 signaling.
It is reported that ALK5 is important for TGFbeta/ALK1 signaling; endothelial cells lacking AlK5 are deficient in TGF beta/ALK 1-induced responses and that theALK5 kinase activity is required for optimal ALK1 activation. Expand
Identification and Functional Characterization of a Smad Binding Element (SBE) in the JunB Promoter That Acts as a Transforming Growth Factor-β, Activin, and Bone Morphogenetic Protein-inducible
The identification of the sequence CAGACA as a direct binding site for Smad proteins will facilitate the identification of regulatory elements in genes that are activated by members of the TGF-β superfamily. Expand
Induction of sonic hedgehog mediators by transforming growth factor-beta: Smad3-dependent activation of Gli2 and Gli1 expression in vitro and in vivo.
It is shown that TGF-beta induces the expression of the Hh signaling molecules Gli1 and Gli2 in various human cell types, including normal fibroblasts and keratinocytes, as well as various cancer cell lines. Expand