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.

Epithelial to mesenchymal transition (EMT) is a continuous process, in which the transition or intermediate states can be molecularly and spatially defined, shedding new light on development and disease EMT.

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.

Inhibiting the RiBi pathway impedes both EMT and MET processes, enhancing chemotherapy efficacy and presenting a novel avenue to tackle advanced breast cancer treatment resistance.