Welcome to the Knowledgebase of the TGF-b/SMAD signaling pathway, KbTSMAD, an information resource of the TGF-b/SMAD signaling pathway and its target gene promoters.

Transforming growth factor-b (TGF-b) proteins regulate cell function and play integral roles in normal development and carcinogenesis via the control of growth, differentiation and apoptosis of cells. Intracellular signaling cascades triggered by these molecules eventually activate transcription factors of the Smad family and others, which in turn, regulate expression of their target genes.

TGF-b inhibits the proliferation of a wide range of cells within the epithelial, endothelial, and hematopoietic lineages, regulates the differentiation of immune, neuronal, mesenchymal, and epithelial cell types, intiates apoptosis in a context-dependent fashion, and plays a role in chromosomal stability.

In neoplastic processes, genetic and epigenetic alterations of the normal TGF-b/SMAD signaling can result in outgrowth and invasion of transformed cells.

Accordingly, the elucidation of the TGF-b/SMAD signaling pathway will, not only, contribute toward characterization of the normal development of the abovementioned cell types, but also, lead toward a better understanding of alterations that ultimately lead to malignancy.

KbTSMAD is an information resource exclusively focused on addressing the need for a better understanding of the TGF-b/SMAD regulatory mechanism. This database currently contains information about the TGF-b/SMAD signaling pathway and its target gene promoters and a map of experimentally known binding sites of SMADs and transcription factors involved in their regulation. A graphical platform, which contains a representative overview of the signaling pathway, is also linked to functional information and regulatory preferences.

Signaling pathway

Expression Data
We currently house only mouse TGF-Beta target genes which were obtained from Yang et al.
Hierarchical model of gene regulation by transforming growth factor beta
Proc Natl Acad Sci U S A, 2003, 100:10269-10274.
Full Text | Supplementary Information

Due to the continuous development and ongoing updates that are performed on this site, we invite you to visit often. Thank you.