hUTP14a降解抑癌基因产物p53，我们近期研究发现：1.Utp14a 基因敲除小鼠死于胚胎E9.5天之前的成血成血管阶段；同时敲除TP53基因未能挽救Utp14a 基因敲除引起的致死，说明Utp14a基因敲除导致胚胎致死存在p53以外的其它通路；在血管内皮中条件性敲除Utp14a后，子代小鼠胚胎死于E9.5之前，胚胎缺乏血管形成，说明Utp14a基因敲除的主要致死原因是血管形成缺失。2.hUTP14a在人肿瘤中表达升高，结合并激活c-Myc；已知c-Myc在肿瘤的血管新生过程中发挥重要作用。本研究将探讨Utp14a在小鼠胚胎成血成血管中的作用、人hUTP14a在肿瘤血管新生中的作用和机制，旨在为肿瘤的发生发展以及转移提供更多理论依据。并为其它血管相关疾病研究和临床诊治提供更多的科学依据和参考靶点。

HUTP14a binds p53 and promotes p53 degradation. We found that Utp14a knockout mice died at E9.5 with failure of vasculogenesis. Knockout of TP53 fails to rescue the embryonic lethality of Utp14a KO mice, indicating that there exits other pathways mediating Utp14a KO lethality rather than p53. The Tie2-Cre conditional knock of Utp14a results in embryo death earlier than E9.5, lacking vasculogenesis, demonstrating that the Utp14a KO embryo died of failure of endothelial cell differentiation. We’re firstly going to verify that Utp14a KO impairs differentiation of vascular endothelial cells during early embryo development of mouse. Further, we’ll uncover the mechanisms by which Utp14a affects differentiation of endothelial cells. We previously found that hUTP14a is upregulated in human tumors. In addition, hUTP14a binds c-Myc and protects c-Myc from degradation. It’s known that c-Myc plays an important roles in hematogenesis and angiogenesis. We thus will unravel if hUTP14a affects the tumor angiogenesis and the involved mechanisms. The purpose of this study is to provide scientific evidence for the function of hUTP14a in the human tumor development, metastasis and other human vascular diseases aiming to offer more potential targets for the clinical treatment of involved diseases.