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.

Integrated live cell imaging and image analyses in the framework of transition path theories identify epithelial-to-mesenchymal transition proceeds through parallel paths.

The transcription factor PROP1 controls a genetic network that drives pituitary stem cells to undergo an epithelial-to-mesenchymal-like transition and differentiate.

BAP1/ASXL is a key regulator of trophoblast invasion during early mouse and human placentation.

Genetic mouse models and human cell lines show that Musashi proteins promote an epithelial/luminal state and inhibit epithelial–mesenchymal transition (EMT), and genome-wide maps of translational regulatory targets connect Musashi proteins to an epithelial alternative splicing program and to the regulation of EMT.

Mammary progenitors identified by a new marker, ICAM-1, undergo epithelial-mesenchymal transition and luminal-to-basal switch in response to paracrine Met activation.

Neuronal progenitor cells autonomously inhibit polarization via the transcription factor Zeb1.

A key Ras-driven signaling pathway stimulates the preferential translation of an effector, EPSTI1, that is both necessary and sufficient for the epithelial-to-mesenchymal transition-like phenotype in colorectal cancer cells.

Overexpression of PLK1 triggers oncogenic transformation and transcriptional reprogramming of prostate epithelial cells, which stimulates cell migration and invasion.

In chick skeletal muscle, an incoming signal leads to two interdependent outcomes: a cell fate change and an epithelial-mesenchymal transition.