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1-4 of 4
Keywords: BMPR1A
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Journal Articles
Journal:
Development
Development (2016) 143 (2): 339–347.
Published: 15 January 2016
... the receptor Bmpr1a in osteoblast lineage cells with Dmp1-Cre, we observed a dramatic increase in trabecular bone mass in postnatal mice, which was due to a marked increase in osteoblast number that was likely to be driven by hyperproliferation of Sp7 + preosteoblasts. Similarly, inducible deletion of Bmpr1a...
Includes: Supplementary data
Journal Articles
Aida Di-Gregorio, Margarida Sancho, Daniel W. Stuckey, Lucy A. Crompton, Jonathan Godwin, Yuji Mishina, Tristan A. Rodriguez
Journal:
Development
Development (2007) 134 (18): 3359–3369.
Published: 15 September 2007
... required for neural induction in the mouse. We have analysed the role of BMP signalling in this process. We demonstrate that prior to gastrulation, Bmp2/4 signalling via Bmpr1a maintains epiblast pluripotency and prevents precocious neural differentiation of this tissue, at least in part by maintaining...
Journal Articles
Deepa Murali, Shunichi Yoshikawa, Rebecca R. Corrigan, Daniel J. Plas, Michael C. Crair, Guillermo Oliver, Karen M. Lyons, Yuji Mishina, Yasuhide Furuta
Journal:
Development
Development (2005) 132 (5): 913–923.
Published: 1 March 2005
... type I receptor gene, Bmpr1a , leads to no detectable eye abnormality. Further reduction of Bmp receptor activity by removing one functional copy of another Bmp type I receptor gene, Bmpr1b , in the retina-specific Bmpr1a mutant background, results in abnormal retinal dorsoventral patterning. Double...
Journal Articles
Thomas Andl, Kyung Ahn, Alladin Kairo, Emily Y. Chu, Lara Wine-Lee, Seshamma T. Reddy, Nirvana J. Croft, Judith A. Cebra-Thomas, Daniel Metzger, Pierre Chambon, Karen M. Lyons, Yuji Mishina, John T. Seykora, E. Bryan Crenshaw, III, Sarah E. Millar
Journal:
Development
Development (2004) 131 (10): 2257–2268.
Published: 15 May 2004
... or absent in mutant follicles. Lef1 expression is maintained, but nuclearβ-catenin is absent from the epithelium of severely affected mutant follicles, indicating that activation of the WNT pathway lies downstream of BMPR1A signaling in postnatal follicles. Mutant hair follicles fail to undergo programmed...