NOTCH-PAX9 signaling in alcohol-induced esophageal injury

项目总结 这份R21提案旨在使用细胞和小鼠模型来理解Noch-PAX9信号的作用 酒精性食道损伤的通路。我们假设乙醇能抑制食道鳞状细胞 通过抑制Noch-PAX9信号通路实现细胞分化。我们计划用两个例子来检验我们的假设 具体目的：(1)确定乙醇是否抑制食道鳞状上皮细胞分化 通过抑制Noch-PAX9信号通路。(2)研究缺口激活是否会产生反作用 酒精引起的食道损伤。这些研究的目的是阐明Noch-PAX9信号在体内的作用。 酒精引起的食道损伤。如果被证明是真的，它将为进一步 激活缺口作为一种新的基于机制的酒精诱导预防措施的研究 食道损伤。

PROJECT SUMMARY This R21 proposal is designed to use cell and mouse models to understand the role of NOTCH-PAX9 signaling pathway in alcohol-induced esophageal injury. We hypothesize that ethanol suppresses esophageal squamous cell differentiation through inhibition of the NOTCH-PAX9 signaling. We plan to test our hypothesis with two specific aims: (1) To determine whether ethanol suppresses esophageal squamous epithelial cell differentiation through inhibition of the NOTCH-PAX9 signaling. (2) To investigate whether NOTCH activation counteracts alcohol-induced esophageal injury. These studies are aimed to elucidate the role of NOTCH-PAX9 signaling in alcohol-induced esophageal injury. If proved true, it will lay down a solid mechanistic foundation to further study NOTCH activation as a novel mechanism-based preventive measure against alcohol-induced esophageal injury.