Sost Deficiency does not Alter Bone’s Lacunar or Vascular Porosity in Mice

SCLEROSTIN (Sost) is expressed predominantly in osteocytes acting as a negative regulator of bone formation. In humans, mutations in the SOST gene lead to skeletal overgrowth and increased bone mineral density, suggesting that SCLEROSTIN is a key regulator of bone mass. The function of SCLEROSTIN as...

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Vydáno v:Front Mater
Hlavní autoři: Mosey, Henry, Núñez, Juan A., Goring, Alice, Clarkin, Claire E., Staines, Katherine A., Lee, Peter D., Pitsillides, Andrew A., Javaheri, Behzad
Médium: Artigo
Jazyk:Inglês
Vydáno: 2017
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Article
On-line přístup:https://ncbi.nlm.nih.gov/pmc/articles/PMC5769812/
https://ncbi.nlm.nih.gov/pubmed/29349060
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.3389/fmats.2017.00027
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