Despite the strides made in understanding the complex network of key regulatory genes and cellular processes that drive palate morphogenesis, patients suffering from these conditions face treatment options that are limited to complex surgeries and multidisciplinary care throughout life. Hence, a better understanding of how molecular interactions drive palatal growth and fusion is critical for the development of treatment and preventive strategies for cleft palates in humans. Our previous work demonstrated that Pax9‐dependent Wnt signaling is critical for the growth and fusion of palatal shelves. We showed that controlled intravenous delivery of small molecule Wnt agonists specifically blocks the action of Dkks (inhibitors of Wnt signaling) and corrects secondary palatal clefts in Pax9^−/− mice. While these data underscore the importance of the functional upstream relationship of Pax9 to the Wnt pathway, not much is known about how the genetic nature of Pax9's interactions in vivo and how it modulates the actions of these downstream effectors during palate formation.

中文翻译：

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Pax9 在小鼠腭发生过程中调节 Wnt 信号的双重作用。

尽管在理解驱动上颚形态发生的关键调控基因和细胞过程的复杂网络方面取得了进展，但患有这些疾病的患者终生面临仅限于复杂手术和多学科护理的治疗选择。因此，更好地了解分子相互作用如何驱动腭生长和融合对于开发人类腭裂的治疗和预防策略至关重要。我们之前的工作表明，依赖Pax9 的Wnt 信号对腭架的生长和融合至关重要。我们表明小分子 Wnt 激动剂的受控静脉内递送特异性阻断 Dkks（Wnt 信号传导抑制剂）的作用并纠正Pax9 中的继发性腭裂^-/-小鼠。虽然这些数据强调了Pax9与 Wnt 通路上游功能关系的重要性，但对Pax9体内相互作用的遗传性质以及它如何在上颚形成过程中调节这些下游效应器的作用知之甚少。