Cleft palate (CP) is a prevalent birth defect that affects one in every 1,000 newborns. Although both genomic and epigenetic factors contribute to the condition, therapies and early diagnoses remain limited because the cause of the problem is still unknown. Inducing CP in animal models relies on the administration of high levels of retinoic acid (RA). A study in Scientific Reports comparing the proteome of Kun Ming control mice and RA-induced CP animals identified 40 differentially expressed proteins. Pathway enrichment analysis helped clarify the functional implications of these differences, identifying the involvement of these proteins in forming and maintaining structural components critical for normal palate development, such as actin and myosin. These findings on the molecular mechanisms associated with CP provide information that can be explored to develop new therapies and diagnostic methods.

Original reference: Huang, Z. et al. Sci. Rep. 14, 21868 (2024)

腭裂 （CP） 是一种普遍的出生缺陷，每 1,000 名新生儿中就有一名受到影响。尽管基因组和表观遗传因素都会导致这种情况，但由于问题的原因仍然未知，因此治疗和早期诊断仍然有限。在动物模型中诱导 CP 依赖于高水平的视黄酸 （RA） 的给药。Scientific Reports 上的一项研究比较了 Kun Ming 对照小鼠和 RA 诱导的 CP 动物的蛋白质组，鉴定出 40 种差异表达蛋白。通路富集分析有助于阐明这些差异的功能意义，确定这些蛋白质参与形成和维持对正常腭发育至关重要的结构成分，例如肌动蛋白和肌球蛋白。这些关于 CP 相关分子机制的发现提供了可以探索以开发新疗法和诊断方法的信息。

原始参考资料：Huang， Z. et al. Sci. Rep.14， 21868 （2024）