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Title: Transcriptional control of Sost in bone

Journal Article · · Bone

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.

Research Organization:
Lawrence Livermore National Laboratory (LLNL), Livermore, CA (United States)
Sponsoring Organization:
USDOE
Grant/Contract Number:
16-ERD-007; AC52-07NA27344
OSTI ID:
1330597
Alternate ID(s):
OSTI ID: 1347664
Report Number(s):
LLNL-JRNL-691682; S875632821630299X; PII: S875632821630299X
Journal Information:
Bone, Journal Name: Bone Vol. 96 Journal Issue: C; ISSN 8756-3282
Publisher:
ElsevierCopyright Statement
Country of Publication:
United States
Language:
English
Citation Metrics:
Cited by: 50 works
Citation information provided by
Web of Science

Cited By (8)

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Conditional Activation of NF‐κB Inducing Kinase (NIK) in the Osteolineage Enhances Both Basal and Loading‐Induced Bone Formation journal July 2019
Updated concept of sarcopenia based on muscle–bone relationship journal October 2019
Deficiency of stress‐associated gene Nupr1 increases bone volume by attenuating differentiation of osteoclasts and enhancing differentiation of osteoblasts journal May 2019
Vitamin D–regulated osteocytic sclerostin and BMP2 modulate uremic extraskeletal calcification journal July 2019
Wnt co-receptors Lrp5 and Lrp6 differentially mediate Wnt3a signaling in osteoblasts journal November 2017
Loss of Myeloid-Specific TGF-β Signaling Decreases CTHRC1 to Downregulate bFGF and the Development of H1993-Induced Osteolytic Bone Lesions journal November 2018