David M. Ornitz

This study shows FGFR1 signaling is essential for osteocyte survival and bone homeostasis by regulating extracellular matrix organization and dendrite formation in maturing osteoblasts.

This study compares hemodynamic and neurohumoral stress in cardiac remodeling, showing that AngII promotes vascular changes while TAC causes myocardial fibrosis.

The paper identifies stress granule coarsening as a critical factor in cardiac electrophysiological dysfunction under oxidative stress.

This study shows LTBP2 promotes TGF-beta signaling and lung fibrosis in mice but is also needed for epithelial repair.

This study shows that the aged muscle tissue environment limits muscle stem cell function, and combined interventions can partially restore muscle mass in aged mice.

This study shows that a mutation in FGF14 causes haploinsufficiency and impairs Purkinje neuron firing, leading to motor and cognitive deficits in mice.

This study shows that proliferation of early and mature osteoblasts is essential for bone fracture healing in mice, as blocking their proliferation leads to fibrous nonunion and reduced callus formation.

The paper investigates FGFR3 expression in human peripheral nervous system tissues and finds no detectable mRNA or protein expression in nerve or dorsal root ganglia, suggesting FGFR3 autoantibodies may not directly cause neuropathy.

The paper identifies biological principles governing postnatal aortic growth, showing it scales with the vertebral column and relies on differentiated cell proliferation rather than stem cells.

This study shows that loss of iFGF14 increases excitability of mature hippocampal and cortical pyramidal neurons by altering INaT voltage-dependence and action potential waveform.

The paper identifies a myofibroblast differentiation program during neonatal lung development using single-cell RNA sequencing and lineage tracing in mice.

This study shows that Fgf9 deletion in tendon disrupts enthesis mineralization by affecting chondrocyte hypertrophy and collagen type X.

This study shows that deletion of Fgf9 in mice leads to enlarged deltoid tuberosities, suggesting a role for Fgf9 in muscle-bone interactions during development.

The paper uses TRAPseq to identify FGF20-regulated genes in mouse organ of Corti progenitors, finding genes involved in hair cell differentiation and hearing loss.

This paper identifies Geminin as a regulator of Hox gene expression in mouse limb development, showing its role in patterning limb skeletal elements through effects on Hox gene expansion and SHH signaling.

This study shows FGF9 and FGF10 use distinct FGFRs and signaling pathways to regulate lung epithelial development and branching.

This paper investigates the interaction between Sox2 and Fgf20 in regulating organ of Corti development, showing their spatially-graded roles in specification and differentiation.

This study shows that loss of FGFR1 and FGFR2 in mature osteoblasts/osteocytes leads to osteocyte death and high bone mass with impaired biomechanical properties in mice.

The paper shows that hair follicle niche precursors are specified before niche formation and requires FGF20 from progenitors.