Results show that STAT3 and KRAS jointly regulate oncogenic dependency of mutant KRAS cancer cells.

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.

Differentiation of CD4 T cells into CD4 T follicular helper cells during viral infection in mice is promoted by tumor growth factor beta.

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.

Distinct interoceptive and gustatory bacterial food cues converge to control neuroendocrine gene expression in two neurons, which modulates and is correlated with internal states driving feeding versus foraging behavior.

Nodal is assumed to be the sole inducer of mesendoderm, but the related signal Vg1 is as essential as Nodal in this process.

Although central nervous system (CNS) regeneration has been considered to be controlled by CNS microenvironment, CNS injury causes leading to leakage of circulating factors into CNS, which promotes CNS regeneration.

Loss of mature β cell identity in diabetes can be prevented and rescued by small molecule inhibitors of the TGFβ pathway.

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.

Ligand capture by cell surface receptor complexes sets the shape of the Nodal signaling pattern in zebrafish.