A pseudokinase in the secretory pathway, Fam20A, activates the real Golgi casein kinase, Fam20C, via a unique mechanism that is lost in human diseases.

KPNB1 regulates rhythmic spatio-temporal nuclear import of the PER/CRY complex and is required for negative feedback repression in mammalian and fly clock function.

The loss of p53 in bone cells activates critical signaling pathways; these are also essential in bone cancer.

L-amino acids are agonists of calcium-sensing receptor, and act jointly with calcium and phosphate ions to control receptor function.

A C-type lectin domain protein is an anabolic growth factor that promotes mesenchymal progenitors in the bone marrow to differentiate into bone cells to maintain skeletal bone mass throughout adult life.

Genetic analyses in mice reveal a communication system between the knee joint and the developing bones that could be explored in studies addressing evolutionary changes in body proportions and in future therapies for growth disorders.

Epigenetic profiling of femoral growth plate chondrocytes helps whittle-down GWAS height variants to fewer putative functional variants.

Fibroblast growth factor induces dephosphorylation and inactivation of the NPR2 guanylyl cyclase, thus decreasing cyclic GMP production in growth plate chondrocytes and contributing to FGF-dependent decreases in bone growth.

Integrin a11 is identified as an Osteolectin receptor, revealing a new mechanism for adult skeletal bone maintenance in which Osteolectin/a11b1 signaling promotes bone formation by activating the Wnt pathway.

A periosteal Bmp2 signaling center couples bone length to bone width during development and must be reactivated by clinical bone anabolic therapies to reduce fracture risk and accelerate fracture repair.