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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. 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 Lab. (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. doi:10.1016/j.bone.2016.10.009.
Sebastian, Aimy, and Loots, Gabriela G. Wed . "Transcriptional control of Sost in bone". United States. doi: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 = {2017},
month = {3}
}

Journal Article:
Free Publicly Available Full Text
Publisher's Version of Record
DOI: 10.1016/j.bone.2016.10.009

Citation Metrics:
Cited by: 5 works
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Works referencing / citing this record:

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