Skeletal defects in Osterix-Cre transgenic mice
Author:
Publisher
Springer Science and Business Media LLC
Subject
Agronomy and Crop Science,Genetics,Animal Science and Zoology,Biotechnology
Link
http://link.springer.com/content/pdf/10.1007/s11248-014-9828-6.pdf
Reference19 articles.
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2. Davey RA, Clarke MV, Sastra S, Skinner JP, Chiang C, Anderson PH, Zajac JD (2012) Decreased body weight in young Osterix-Cre transgenic mice results in delayed cortical bone expansion and accrual. Transgenic Res 21(4):885–893
3. Greenblatt MB, Shim JH, Zou W, Sitara D, Schweitzer M, Hu D, Lotinun S, Sano Y, Baron R, Park JM, Arthur S, Xie M, Schneider MD, Zhai B, Gygi S, Davis R, Glimcher LH (2010) The p38 MAPK pathway is essential for skeletogenesis and bone homeostasis in mice. J Clin Invest 120(7):2457–2473
4. Kamiya N, Ye L, Kobayashi T, Mochida Y, Yamauchi M, Kronenberg HM, Feng JQ, Mishina Y (2008) BMP signaling negatively regulates bone mass through sclerostin by inhibiting the canonical Wnt pathway. Development 135(22):3801–3811
5. Komori T, Yagi H, Nomura S, Yamaguchi A, Sasaki K, Deguchi K, Shimizu Y, Bronson RT, Gao YH, Inada M, Sato M, Okamoto R, Kitamura Y, Yoshiki S, Kishimoto T (1997) Targeted disruption of Cbfa1 results in a complete lack of bone formation owing to maturational arrest of osteoblasts. Cell 89(5):755–764
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