High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
about
Betacellulin inhibits osteogenic differentiation and stimulates proliferation through HIF-1alphaEGF receptor ligands: recent advancesProstate cancer derived prostatic acid phosphatase promotes an osteoblastic response in the bone microenvironment.Amphiregulin-EGFR signaling mediates the migration of bone marrow mesenchymal progenitors toward PTH-stimulated osteoblasts and osteocytes.Epidermal growth factor receptor plays an anabolic role in bone metabolism in vivo.Signaling pathways affecting skeletal health.Klotho Lacks an FGF23-Independent Role in Mineral Homeostasis.The critical role of the epidermal growth factor receptor in endochondral ossification.Stanozolol Decreases Bone Turnover Markers, Increases Mineralization, and Alters Femoral Geometry in Male Rats.Augmented Fibroblast Growth Factor-23 Secretion in Bone Locally Contributes to Impaired Bone Mineralization in Chronic Kidney Disease in Mice.
P2860
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P2860
High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
description
2009 nî lūn-bûn
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2009年の論文
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name
High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
@en
High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
@nl
type
label
High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
@en
High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
@nl
prefLabel
High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
@en
High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
@nl
P2093
P50
P356
P1476
High cortical bone mass phenotype in betacellulin transgenic mice is EGFR dependent.
@en
P2093
Bettina Mayer-Roenne
Maik Dahlhoff
Reinhold G Erben
Verena Proell
P304
P356
10.1359/JBMR.081202
P577
2009-03-01T00:00:00Z