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.

The acquisition of vascular quiescence during transition to adulthood is driven by distinct transcriptional and epigenetic programs of pro- and anti-angiogenic genes, with the most prominent effect on the suppression of TGFß family signaling.

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.

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.

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.

Low expression of Cbfb may be the cause of osteoarthritis, and local admission of Cbfb may rescue and protect against osteoarthritis through decreasing Wnt/β-catenin signaling, and increasing Hippo/Yap signaling and Tgfβ/Smad2/3 signaling in osteoarthritis articular cartilage.

Unbiased single-cell RNAseq data analysis combined with mouse genetic approaches reveal that TGF-β signaling and perimysial-specific regulators may cooperatively define perimysial-to-myogenic signals in regulating pharyngeal myogenesis.

Overexpression of VPS9D1-AS1 is a lncRNA to activate TGF-β and IFN signaling pathways, regulates crosstalk between cancer cells and T lymphocytes in the tumor microenvironment.