Anomalous expression of the testis protein ZNF165 in cancer cells promotes assembly of a neomorphic transcriptional complex that modulates transcription of TGFβ target genes to support tumor cell survival.
TGFß signaling regulates migration of tenogenic cells from Scx- and non-Scx lineages and is required for functional regeneration after neonatal tendon injury.
TGFβ signaling to retinal microglia is central to the regulation of neuroinflammatory responses relevant to age-related macular degeneration (AMD), a leading cause of blindness in the developed world.
Conditional deletion of TGFβ signaling results in tenocyte dedifferentiation in vivo demonstrating a key role for TGFβ signaling in the maintenance of the tendon cell fate.
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.
Alk5/TGF-β signaling is required in the endothelium to orchestrate zebrafish cardiac outflow tract morphogenesis, regulating smooth muscle cell and extracellular matrix organization.
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.
