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. Furthermore we review the current understanding of the upstream molecular mechanisms that regulate Sost/SOST transcription, in bone.
- Authors:
- Publication Date:
- Research Org.:
- Lawrence Livermore National Laboratory (LLNL), Livermore, CA (United States)
- Sponsoring Org.:
- USDOE
- OSTI Identifier:
- 1330597
- Alternate Identifier(s):
- OSTI ID: 1347664
- Report Number(s):
- LLNL-JRNL-691682
Journal ID: ISSN 8756-3282; S875632821630299X; PII: S875632821630299X
- Grant/Contract Number:
- 16-ERD-007; AC52-07NA27344
- Resource Type:
- Published Article
- Journal Name:
- Bone
- Additional Journal Information:
- Journal Name: Bone Journal Volume: 96 Journal Issue: C; Journal ID: ISSN 8756-3282
- Publisher:
- Elsevier
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 59 BASIC BIOLOGICAL SCIENCES
Citation Formats
Sebastian, Aimy, and Loots, Gabriela G. Transcriptional control of Sost in bone. United States: N. p., 2017.
Web. doi:10.1016/j.bone.2016.10.009.
Sebastian, Aimy, & Loots, Gabriela G. Transcriptional control of Sost in bone. United States. https://doi.org/10.1016/j.bone.2016.10.009
Sebastian, Aimy, and Loots, Gabriela G. Wed .
"Transcriptional control of Sost in bone". United States. https://doi.org/10.1016/j.bone.2016.10.009.
@article{osti_1330597,
title = {Transcriptional control of Sost in bone},
author = {Sebastian, Aimy and Loots, Gabriela G.},
abstractNote = {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. Furthermore we review the current understanding of the upstream molecular mechanisms that regulate Sost/SOST transcription, in bone.},
doi = {10.1016/j.bone.2016.10.009},
journal = {Bone},
number = C,
volume = 96,
place = {United States},
year = {Wed Mar 01 00:00:00 EST 2017},
month = {Wed Mar 01 00:00:00 EST 2017}
}
https://doi.org/10.1016/j.bone.2016.10.009
Web of Science
Works referencing / citing this record:
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