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Overexpression of Shox2 Leads to Congenital Dysplasia of the Temporomandibular Joint in Mice

Our previous study reported that inactivation of Shox2 led to dysplasia and ankylosis of the temporomandibular joint (TMJ), and that replacing Shox2 with human Shox partially rescued the phenotype with a prematurely worn out articular disc. However, the mechanisms of Shox2 activity in TMJ developmen...

詳細記述

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書誌詳細
主要な著者: Li, Xihai, Liang, Wenna, Ye, Hongzhi, Weng, Xiaping, Liu, Fayuan, Liu, Xianxiang
フォーマット: Artigo
言語:Inglês
出版事項: MDPI 2014
主題:
オンライン・アクセス:https://ncbi.nlm.nih.gov/pmc/articles/PMC4159784/
https://ncbi.nlm.nih.gov/pubmed/25062348
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.3390/ijms150813135
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