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.

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.

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.

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.

Cartilage and bone tumors arise from chondrocyte or osteoblast progenitors but not differentiated cells or multipotent mesenchymal stem cells (MSCs) via the IHH-Wnt/β-Catenin pathway.

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.

How does the skeleton detect and adapt to changes in the mechanical load it has to carry?

A group of cells that can become adipocytes controls the formation of blood vessels in the bone marrow, and also regulates the differentiation of resident mesenchymal progenitor cells.

The major protein disulfide isomerase family member, PDIA1, is essential in beta cells of mice fed a high-fat diet to maintain glucose homeostasis, proinsulin maturation and organelle integrity.

Def6 functions as a novel immunoregulator in bone cells via endogenous type-I interferon response to regulate bone remodeling.