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Ablation of canonical TGFβ signaling in muscle stem cells at any age is detrimental, and not beneficial, to effective skeletal muscle regeneration due to the promotion of premature fate commitment at the expense of progenitor amplification.

A new mechanism connects the loss of TGFβ signaling with invasion and metastasis in highly malignant transition zone tumors.

TGFβ family members instruct a cell fate decision downstream of stochastic signaling in the Drosophila retina to ensure correct pairing between different color photoreceptors for color vision.

TGFβ and serotonin signaling in a neural circuit encodes food availability; these signals regulate the dynamic range and variability on the circuit to impact coding accuracy and lifespan responses.

Calcium channel blockers accelerate aortic aneurysm and cause premature aortic rupture in a mouse model of Marfan syndrome through protein kinase C-mediated activation of extracellular signal-regulated kinase.

Live cell imaging demonstrates that the dynamics of ligand presentation influence signaling through two closely related morphogen signaling pathways in dramatically different ways.

C. elegans nematodes use a sensory-neuronal circuit to determine whether to defend themselves from hydrogen peroxide attack or to freeload off orthologous protective defenses from bacteria in their surrounding environment.

Perturbation of mechanical force at muscle attachments and its effects on tendon morphogenesis provides insights into the mechanisms underlying cellular responses to tensional force and resulting extracellular matrix production.

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.

The acquisition of vascular quiescence during transition to adulthood is driven by distinct transcriptional and epigenetic programs of pro- and anti-angiogenic genes, with the most prominent effect on the suppression of TGFß family signaling.