摘要
肿瘤蛋白p53诱导的核蛋白2(TP53INP2),也称糖尿病与肥胖调控蛋白(DOR),在骨骼肌、心肌和脑等代谢旺盛的组织中表达水平较高。TP53INP2在细胞核内主要发挥转录辅激活因子的作用,如作为甲状腺激素受体的辅激活因子调控甲状腺激素相关基因的表达。后续研究发现,TP53INP2为细胞内重要的分解代谢途径—细胞自噬所必需,饥饿时TP53INP2出核参与自噬的起始。在骨骼肌中,TP53INP2通过促进自噬导致肌肉流失,而在白色脂肪组织中,TP53INP2则通过促进自噬抑制脂肪前体细胞的分化。此外,在营养丰富的条件下,TP53INP2能够定位于核仁,协助r DNA转录起始前复合物的组装,促进r DNA的转录,参与细胞内重要的合成代谢—核糖体的生物发生。临床统计数据表明,TP53INP2的表达水平与糖尿病和某些类型的癌症早期的发生发展密切相关。本文对TP53INP2在转录调控、细胞自噬和相关疾病如癌症与糖尿病中的生物学功能进行综述。
Tumor protein 53-induced nuclear protein 2（ TP53 INP2）,also known as diabetes and obesity regulated protein（ DOR）,is highly expressed in metabolically active tissues. TP53 INP2 was identified as a co-activator of a variety of nuclear receptors（ NRs） including thyroid hormone receptors. In response to nutrient deprivation, nuclear TP53 INP2 translocates to the cytoplasm to participate in autophagy initiation. In the mouse model, TP53 INP2 promotes skeletal muscle wasting and suppresses adipogenesis. Recently,TP53 INP2 was reported to be localized in the nucleolus and promote ribosome biogenesis through stimulating ribosomal DNA transcription. Clinically, TP53 INP2 seems to be a biomarker for the early diagnosis of cancer and diabetes mellitus development. This article reviews the biological functions of TP53 INP2 in transcription regulation,autophagy and related diseases such as cancer and diabetes.
作者
许银丰
李宁
陈颖卓
XU Yin-Feng;LINing;CHEN Ying-Zhuo(Laboratory of Basic Biology,Hunan First Normal University,Changsha 410205,China;Department of Biochemistry and Molecular Biology,Basic Medical College,Qingdao University,Qingdao 266071,China)
出处
《中国生物化学与分子生物学报》
CAS
CSCD
北大核心
2018年第11期1146-1153,共8页
Chinese Journal of Biochemistry and Molecular Biology
基金
国家自然科学基金项目(No.31701213)
湖南省自然科学基金项目(No.2017JJ3047)
湖南省教育厅科学研究优秀青年项目(No.17B056)资助~~
