朱雅茜

副教授 硕士生导师

所在单位:基础医学院

学历:博士研究生毕业

办公地点:湖南省长沙市岳麓区桐梓坡路172号中南大学湘雅医学院孝骞楼5楼病理生理学教研室

性别:女

联系方式:zhu_yaxi@csu.edu.cn

学位:医学博士学位

在职信息:在职

其他任职:湖南省病理生理学会理事,湖南省内分泌学专业委员会青年委员会委员

毕业院校:中南大学

学科:基础医学

曾获荣誉:

2022-09-30  当选:  湖南省“三尖”创新人才工程青年科技人才(荷尖)

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PDX1, Neurogenin-3, and MAFA: critical transcription regulators for beta cell development and regeneration

发布时间:2023-02-27

点击次数:

发表刊物:Stem Cell Res Ther

关键字:Diabetes; Embryonic stem cells; Induced pluripotent stem cells; Regenerative medicine; Trans-differentiation.

摘要:Transcription factors regulate gene expression through binding to specific enhancer sequences. Pancreas/duodenum homeobox protein 1 (PDX1), Neurogenin-3 (NEUROG3), and V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MAFA) are transcription factors critical for beta cell development and maturation. NEUROG3 is expressed in endocrine progenitor cells and controls islet differentiation and regeneration. PDX1 is essential for the development of pancreatic exocrine and endocrine cells including beta cells. PDX1 also binds to the regulatory elements and increases insulin gene transcription. Likewise, MAFA binds to the enhancer/promoter region of the insulin gene and drives insulin expression in response to glucose. In addition to those natural roles in beta cell development and maturation, ectopic expression of PDX1, NEUROG3, and/or MAFA has been successfully used to reprogram various cell types into insulin-producing cells in vitro and in vivo, such as pancreatic exocrine cells, hepatocytes, and pluripotent stem cells. Here, we review biological properties of PDX1, NEUROG3, and MAFA, and their applications and limitations for beta cell regenerative approaches. The primary source literature for this review was acquired using a PubMed search for articles published between 1990 and 2017. Search terms include diabetes, insulin, trans-differentiation, stem cells, and regenerative medicine.

合写作者:Liu Q, Zhou Z

第一作者:Yaxi Zhu

论文类型:期刊论文

通讯作者:Ikeda Y.

卷号:8

期号:(1)

页面范围:240

是否译文:

发表时间:2017-11-02

收录刊物:SCI

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