Micropatterned differentiation of mouse pluripotent stem cells gives rise to regionally distinct cell types arising in embryos at gastrulation.

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

Members of the BMP family of growth factors act as a reiterative code of distinct activities to direct the identities of different classes of sensory neurons in the spinal cord.

Identifying the pathways that support human naive-state pluripotent stem cells provides insights into the signalling-based regulation of human pluripotency and enables informed decisions to improve conditions for pluripotent cell culture.

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.

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.

During vertebrate axial extension, the tail bud originates from the activation of a developmental module in a subset of axial progenitors, concurrent but different to gastrulation.

Combination of in vitro and in vivo approaches reveal how learning suppresses the microRNA system to trigger de novo synthesis of plasticity proteins, a missing link in the current model of microRNA-mediated translation in persistent synaptic plasticity and memory.

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

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.