title: Transcriptional control of Sost in bone.
abstract: Sclerostin is an osteocyte derived negative regulator of bone formation. A highly specific expression pattern and the exclusive bone phenotype have made Sclerostin an attractive target for therapeutic intervention in treating metabolic bone diseases such as osteoporosis and in facilitating fracture repair. Understanding the molecular mechanisms that regulate Sclerostin transcription is of great interest as it may unveil new avenues for therapeutic approaches. Such studies may also elucidate how various signaling pathways intersect to modulate bone metabolism. Here we review the current understanding of the upstream molecular mechanisms that regulate Sost/SOST transcription, in bone.
authors: Biology and Biotechnology Division, Lawrence Livermore National Laboratory, 7000 East Avenue, L-452, Livermore, CA 94550, USA; School of Natural Sciences, University of California, Merced, CA 95343, USA.
authors: Aimy
authors: A
authors: Sebastian
authors: Biology and Biotechnology Division, Lawrence Livermore National Laboratory, 7000 East Avenue, L-452, Livermore, CA 94550, USA; School of Natural Sciences, University of California, Merced, CA 95343, USA. Electronic address: Loots1@llnl.gov.
authors: Gabriela G
authors: GG
authors: Loots
mesh_terms: D000818:Animals; D019485:Bone Morphogenetic Proteins / Q000235:genetics* / Q000378:metabolism; D001842:Bone and Bones / Q000378:metabolism*; D005786:Gene Expression Regulation; D006801:Humans; D014018:Tissue Distribution; D014158:Transcription, Genetic
chemical_list: D019485:Bone Morphogenetic Proteins