个人信息
教师姓名:肖德胜

学位:博士学位

学历:研究生(博士)毕业

职称:教授

所在单位:基础医学院

学术荣誉: 曾获荣誉:
个人简介

    中南大学教授,博士生/博士后导师,现任中南大学基础医学院病理学系/湘雅医院病理科副主任、分子病理诊断中心主任。病理学国家级精品课程主讲教师、病理学国家级资源共享课程主讲教师及基础医学形态学国家级教学团队、卫计委临床重点专科骨干成员,副主编及参编《病理学》全国高等学校医学规划教材及配套教材7本,人民卫生出版社国家医学教育题库病理学学科副主编,获校级教学成果奖8项;参与或主持了教育部教改项目、教育部修购专项资助项目、教育部985资助项目、国家自然科学基金及湖南省科技计划项目10项。发表本专业SCI论文90余篇。获湖南省自然科学奖三等奖一项。

Desheng Xiao, Ph.D., professor, PhD candidate/post-doctoral supervisor, Deputy Director of Department of Pathology, Basic Medical School/Xiangya Hospital, Central South University, Director of Molecular Pathology Diagnosis Center.  The main teacher of national excellent pathology course and national resource sharing course, the national teaching team of basic medical Morphology, and the main member of National Health and Family Planning Commission key clinical specialty.  Presided over or participated in 10 projects of national Natural Science Foundation of China and Natural Science Foundation of Hunan Province. Won the third prize of Natural Science award of Hunan Province (ranked the third).  Published more than 90 SCI papers in this field.  Concurrently hold the molecular pathology group member of the Chinese medical doctor association pathology branch, a member of the standing committee of the China medical equipment AI union pathology committee, the incoming chairman of hunan province medical association pathology professional committee, the chairman of hunan medical association pathology professional committee Younger Committee, the vice president of Hunan Medical Doctor Association Pathologist Branch, the vice director of hunan Clinicopathological Quality Control Center, a member of Hunan Anti-cancer Association Lung Cancer Professional Committee. and a review expert of the National Natural Science Foundation of China.



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DNA methylation modifier LSH inhibits p53 ubiquitination and transactivates p53 to promote lipid metabolism


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影响因子:4.237

所属单位:中南大学

教研室:病理学系

发表刊物:Epigenetics Chromatin

关键字:DUB; LSH; Lipid metabolism; P53; PKM2

摘要:Background: The stability of p53 is mainly controlled by ubiquitin-dependent degradation, which is triggered by the E3 ubiquitin ligase MDM2. The chromatin modifier lymphoid-specific helicase (LSH) is essential for DNA methylation and cancer progression as a transcriptional repressor. The potential interplay between chromatin modifiers and transcription factors remains largely unknown. Results: Here, we present data suggesting that LSH regulates p53 in cis through two pathways: prevention proteasomal degradation through its deubiquitination, which is achieved by reducing the lysine 11-linked, lysine 48-linked polyubiquitin chains (K11 and K48) on p53; and revival of the transcriptional activity of p53 by forming a complex with PKM2 (pyruvate kinase 2). Furthermore, we confirmed that the LSH-PKM2 interaction occurred at the intersubunit interface region of the PKM2 C-terminal region and the coiled-coil domains (CC) and ATP-binding domains of LSH, and this interaction regulated p53-mediated transactivation in cis in lipid metabolism, especially lipid catabolism. Conclusion: These findings suggest that LSH is a novel regulator of p53 through the proteasomal pathway, thereby providing an alternative mechanism of p53 involvement in lipid metabolism in cancer.

合写作者:Ying Shi, Na Liu, Zuli Wang, Rui Yang, Bin Yan, Xiaoli Liu, Weiwei Lai,Yating Liu, Desheng Xiao, Hu Zhou, Yan Cheng, Ya Cao, Shuang Liu

第一作者:Ling Chen

论文类型:期刊论文

通讯作者:Zanxian Xia, Yongguang Tao

期号:12(1)

页面范围:59

是否译文:

发表时间:2019-10-08

收录刊物:SCI


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