Identifying genes that regulate bone remodeling as potential therapeutic targets.
Bone remodeling, a coupled process involving bone resorption and formation, is initiated by mechanical signals and is controlled by local and systemic factors that regulate osteoblast and osteoclast differentiation and function. An excess of resorption over formation leads to the bone loss and increased propensity to fracture that is characteristic of osteoporosis. A newly described inhibitor of osteoblast differentiation, Ciz, interferes with bone morphogenic protein signaling. As a consequence, Ciz-deficient mice develop increased bone mass.
Krane
Stephen M
SM
Harvard Medical School and Massachusetts General Hospital, Boston, MA 02129, USA. krane.stephen@mgh.harvard.edu
D000818:Animals; D016723:Bone Remodeling / Q000235:genetics / Q000502:physiology; D001862:Bone Resorption / Q000235:genetics / Q000523:psychology; D005786:Gene Expression Regulation; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D010006:Osteoblasts / Q000502:physiology; D010010:Osteoclasts / Q000502:physiology; D010012:Osteogenesis / Q000235:genetics / Q000502:physiology; D010024:Osteoporosis / Q000235:genetics / Q000503:physiopathology; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D015534:Trans-Activators / Q000235:genetics* / Q000378:metabolism
D015534:Trans-Activators; C498621:ZNF384 protein, human