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.

Alk5/TGF-β signaling is required in the endothelium to orchestrate zebrafish cardiac outflow tract morphogenesis, regulating smooth muscle cell and extracellular matrix organization.

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.

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.

The proper mechanical stimulus could promote the migration of Prrx1⁺ cells to the injury site to enhance enthesis injury repair.

Detailed analysis of transporter expression and glucose uptake rates shows that carbohydrate import at the blood–brain barrier is adapted via TGF-βsignaling-dependent transcriptional regulation of carbohydrate transporters to protect the brain form effects of nutrient shortage.

Phenotypic diversity and cell state transition (i.e., acquisition of a CD44+/CD24- cell state or exposure to TGF-beta) can spur intra-tumor genetic heterogeneity and contribute to acquired resistance.

The C. elegans canonical DBL1/TGFβ signaling pathway is not only regulated in response to bacterial challenges, but also appropriately tailors behaviors and molecular immune responses to bacterial challenges, and animals lacking DBL1 respond to specific bacteria as more harmful.

Muscle hypertrophy and regeneration are critically regulated by combination of TGF-β type I receptors in myofibres.