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

Activin class member, activin C, is a canonical TGFβ family member that signals through the type I receptor, action receptor-like kinase 7 and is resistant to follistatin antagonism.

Diversification of human pacemaker subpopulations is directed by WNT and TGFβ signaling.

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

Tgfb3 inhibits Muller glial cell reprogramming and drives Muller cell quiescence in the injured zebrafish retina, thereby inhibiting retina regeneration.

Cells control the spatial organization and signaling of TGFβ receptors at focal adhesions via a mechanically regulated mechanism to integrate biochemical and physical cues.

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.

Ribosome profiling and loss-of-function during human ESC pancreatic differentiation reveal abundant lncRNA translation and an essential role for translated LINC00261 in beta cell differentiation, likely through a trans-regulatory, microprotein-independent mechanism.

The signaling requirements to decouple proliferation of pancreatic progenitors from differentiation were elucidated and employed for the reproducible expansion, under GMP-compliant conditions, of pancreatic progenitors derived from different human pluripotent stem cell lines.

Thermal injury and infected wounds induce distinct inflammatory and remodeling mechanisms that alter the dynamics of wound repair.