Mice that lacked the genes for the bone protein osteocalcin were generated and were used to study the function of osteocalcin. These osteocalcin-deficient mutants had normal bones at birth but had increased bone density and thickness at 6 months. Their osteoblasts deposited more bone matrix than those of wild-type mice, though mineralization was not affected. Osteocalcin, therefore, was concluded to be a negative regulator of bone formation.
No takes yet. Share an insight, caveat, or question.
George Wolf (2009) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context: