The active small G protein, Arl15-GTP, interacts with the MH2 domain of Smad4 and positively regulates the TGFß family signaling pathway by promoting the assembly of the Smad-complex.

Promoter studies identified BMP/Smad signaling as a transcriptional regulator of Ppif gene encoding cyclophilin D, a component of the mitochondrial permeability transition pore, and gain- and loss-of-function experiments determined how such regulation affects osteogenic differentiation.

The requirement for WNT signaling in mesendoderm differentiation is temporally separate from that of ACTIVIN signaling and acts to switch the output of ACTIVIN/SMAD2 from pluripotency maintenance to mesendoderm patterning.

SMAD1/5 signaling is essential for the full transforming growth factor β (TGF-β)-induced transcriptional program and physiological responses and is induced via a novel receptor activation mechanism, involving two distinct type I receptors.

Cells control the spatial organization and signaling of TGFβ receptors at focal adhesions via a mechanically regulated mechanism to integrate biochemical and physical cues.

NODAL/Activin-induced SMAD2 binding directly drives remodeling of both open and closed chromatin and does not directly correlate with temporal patterns of gene expression upon prolonged signaling.

The Hippo signaling restricts the number of SHF cardiomyocytes in the venous pole by negatively regulating Bmp-Smad signaling in the cells of lateral plate mesoderm.

Pathogen-specific CTLs are programmed to provide customized responses against infection, by inflammatory molecules that promote localization in peripheral and lymphoid tissues using alternative signaling mechanisms.

SMOC inhibits BMP signaling locally, but also expands the range of BMP signaling by competing for heparan sulfate binding sites.

Multiple levels of gene regulation in the TGFβ signaling pathway mediate the expression of Mmp13, establish species-specific domains of bone resorption, and likely generate evolutionary variation in jaw length.