This figure outlines the role of KLF10 protein as a target and as a regulator of the TGFBeta-Smad 2,3 signaling pathway

This figure outlines the role of KLF10 protein as a target and as a regulator of the TGFβ-Smad 2,3 signaling pathway. TGFβ binds to its membrane receptors (R2 R1) to activate the Smad signaling pathway. KLF10 (TIEG) is one of the rapid, early response genes whose expression is activated. KLF10 mRNA is rapidly translated into the KLF10 protein, which as a gene transcription repressor inhibits Smad 7 gene expression and, as a gene activator, induces Smad 2 gene expression. The ultimate outcome is a continued activation of the TGFβ-Smad signaling pathway, that is, an extension of the signaling period. The KLF10 mRNA and protein are rapidly turned over, thus the signaling is fine tuned to the KLF10 levels and activity. The steroid, estrogen (E), also induces the expression of KLF10 gene transcription, which is one mechanism of the well documented crosstalk between TGFβ and estrogen signaling.

Publication

Functional role of KLF10 in multiple disease processes. () Malayannan Subramaniam, et al. Biofactors. ;36(1):8-18. Figure: F2. All organisms Mus musculus Homo sapiens Gallus gallus

Disease mentions