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.

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 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.

Mouse models reveal fundamental roles of SMAD1/5 in mediating both bone morphogenetic protein signaling pathways and the transcriptional response to progesterone during decidualization.

GAS5 is related to osteoporosis by regulating the differentiation of bone marrow stromal cells that acts as a promising treatment target for osteoporosis.

Depletion of the TGFβ signal-transducer, SMAD4, in granulosa cells of growing follicles reduces the number of filopodia, termed transzonal projections, that stably attach to and mediate communication with the oocyte.

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.

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.

The mechanism underlying Shprintzen–Goldberg syndrome is solved and reveals that missense mutations in the transcriptional repressor SKI abolish ligand-induced SKI degradation, which results in attenuation of TGF-β transcriptional responses.