Joseph Heitman.
Joseph Heitman.
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约瑟夫·海特曼。
DOI：
10.1016/j.cub.2021.12.046
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发表时间：
2022
期刊：
影响因子：
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通讯作者：
Heitman,Joseph
中科院分区：
文献类型：
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作者：
Heitman,Joseph
约瑟夫·海特曼就是詹姆斯·B。杜克大学分子遗传学和微生物学系主任兼杜克教授，他研究模型和致病真菌作为模型，以了解基本的生物学问题和未满足的医疗需求。他在芝加哥大学学习化学和生物化学（1980-1984年），在康奈尔大学和洛克菲勒大学接受医学博士和博士课程培训，与Peter Model和Norton Zinder一起研究细菌限制修饰系统和DNA修复，并与Michael Hall一起在瑞士巴塞尔的Biozentrum担任EMBO研究员。Heitman和Hall与Sandoz/Novartis的Rao Movva合作研究发现FKBP 12和TOR是免疫抑制性抗真菌天然产物雷帕霉素的靶点。Heitman于1992年加入杜克大学，他的研究项目主要集中在真核微生物病原体通过单性生殖的进化，以及涉及RNAi依赖性表位突变的新型耐药机制。他是美国微生物学会、美国艺术与科学学会和美国国家科学院的成员。
Joseph Heitman is James B. Duke Professor and Chair of the Department of Molecular Genetics and Microbiology at Duke University, and he studies model and pathogenic fungi as models to understand fundamental biological questions and unmet medical needs. He studied chemistry and biochemistry at the University of Chicago (1980–1984), trained in the MD–PhD program at Cornell and Rockefeller Universities, working with Peter Model and Norton Zinder on bacterial restriction–modification systems and DNA repair, and was an EMBO Fellow with Michael Hall at the Biozentrum in Basel, Switzerland. Collaborative studies by Heitman and Hall with Rao Movva at Sandoz/Novartis led to the discovery of FKBP12 and TOR as the targets of the immunosuppressive antifungal natural product rapamycin. Heitman joined the Duke faculty in 1992, and his research program focuses on the evolution of eukaryotic microbial pathogens via unisexual reproduction, and novel drug resistance mechanisms involving RNAi-dependent epimutations. He is a member of the American Academy of Microbiology, the American Academy of Arts and Sciences, and the National Academy of Sciences.