The collinear activation of a subset of posterior Hox genes is responsible for establishing a Wnt/T activity gradient that is required to generate the complete body axis, and hence the full set of segments within a vertebrate embryo.

Genetic and anatomical analyses of Hox gene function uncover a limb-independent program of sensory neuron fate specification and connectivity.

Molecular, genetic, and behavioral assays in mice establish a new role for Hox proteins in the final steps of spinal motor neuron development.

Chondrocytes derived from induced pluripotent stem cells with the dysplasia-causing TRPV4 mutations, V620I and T89I mutation, were resistant to BMP4-induced hypertrophy, suggesting a mechanism underlying the effects of TRPV4 dysfunction on the severity of skeletal dysplasia.

A key molecule that connects leukemogenic proteins to aberrant HOX gene regulation turned out to be a nuclear export factor, CRM1.

Discovering that Hoxb1 acts as a repressor of cardiac differentiation on second heart field progenitor cells helps us to understand the etiology of congenital heart defects such as atrioventricular septal defects.

A genome-wide CRISPR/Cas9 knockout screening approach identified C/EBPδ as transcriptional regulator of the alarmins S100A8 and S100A9 during differentiation of monocytes and inflammatory processes in vivo.

Hox genes are activated sequentially and, at the same time, undergo a transition from an inactive to an active chromatin compartment, most likely to prevent posterior genes being activated too early.