Piezo1 functions as a key mechanotransducer for conferring mechanosensitivity to osteoblasts and determining mechanical-load-dependent bone formation, and represents a novel therapeutic target for treating osteoporosis or unloading-induced severe bone loss.

Live imaging and genetic analyses revealed that notochord vacuoles play a critical role in spine morphogenesis by absorbing vertebral bone growth, thus implicating notochord mechanics in congenital scoliosis.

Simultaneous inhibition of two distinct kinase targets stimulates bone formation without concurrently increasing bone resorption, therefore representing a promising new treatment strategy for osteoporosis.

Akt mediated S14 phosphorylation of Id2 augments its protein stability and growth cone localization, promoting growth cone formation and axon growth in the developing neuron and contributing to axon regeneration in the damaged hippocampus slice.

Mechanical loading and the bone anabolic action of parathyroid hormone result in rapid, lysosomal degradation of sclerostin protein, revealing physiologically important post-translational control of this critical regulator of bone formation.

In vitro and in vivo studies highlight the dual regulatory effects that 7,8-dihydroxyflavone exerts on bone formation and resorption.

Correlating changes in structure and gene expression in cone photoreceptors of mice daily, between birth and eye opening, created a resource that supports research in photoreceptor function, development, transplantation and repair.

Mechanosensitive channels Piezo1/2 are required for osteoblast differentiation from progenitors by sensing fluid sheer stress and matrix rigidity and regulating NFATc1, YAP1 and ß-catenin activities through Ca²⁺ stimulated phosphatase calcineurin.

Mechanical stimuli activate Piezo1 in osteoblast lineage cells and thereby promote bone formation in part via Wnt1.

Nascent regulatory peptides tune the translation rate through a continuous, dynamic reshaping of the functional center of the ribosome.