基本信息
教育经历
工作经历
研究概述
发表文章

蒋辉 博士

北京生命科学研究所研究员

Hui Jiang, Ph.D. Assistant Investigator, NIBS, Beijing, China

Phone: -8620

Email: jianghui@nibs.ac.cn




教育经历
Education
2008 中科院神经科学研究所神经生物学博士
Ph.D., Institute of Neuroscience, SIBS, CAS, China

2001 南京大学生物化学系生物化学学士
B.S., Department of Biochemistry, Nanjing University, China


工作经历
Professional Experience
2016- 北京生命科学研究员
Assistant Investigator, National Institute of Biological Sciences, Beijing, China

2011-2016 北京生命科学研究所Fellow
NIBS fellow, National Institute of Biological Sciences, Beijing, China

2008-2011 美国得克萨斯大学西南医学中心博士后
Postdoctoral researcher, UT Southwestern Medical Center at Dallas, USA



研究概述
Research Description
蒋辉实验室主要研究线粒体质量控制和稳态维持的分子机制。线粒体功能紊乱与许多疾病发生高度相关。线粒体功能下降和损伤的积累被认为是衰老和衰老相关疾病发生的重要诱因之一。利用酵母，培养细胞，和基因修饰的小鼠等模型，我们致力于揭示监测和维持线粒体质量的分子机制。
线粒体外膜拥有诸多蛋白复合物，这些复合物执行着线粒体蛋白输入，融合/分裂的动态平衡，线粒体自噬等重要的信号传导和代谢功能。目前外膜蛋白组的质量控制机制仍知之甚少。利用酵母这一模式生物，我们融合遗传和生化手段去发现调节外膜蛋白降解的关键分子并阐明其生化机理。
线粒体融合与分裂的动态平衡(mitochondrial fusion/fission dynamics)对线粒体功能至关重要，多个调控mitochondria dynamics 的分子突变导致严重的神经和肌肉组织退行性病变（如OPA1, Mfn2和Drp1等）。线粒体过度分裂(over-fission)普遍存在于退行性病变中。我们致力于发展调控mitochondria dynamics的小分子化合物及其在疾病模型上的应用。
超过99％的线粒体蛋白是由核基因编码，并在细胞质中表达的。线粒体与它所处的环境之间的密切交流对维持线粒体的稳态平衡至关重要。我们致力于阐明细胞在线粒体功能受损时（如呼吸链缺失等）的适应性变化及其功能。

Dr. Hui Jiang’s laboratory is interested in studying the quality control and homeostatic mechanisms of mitochondria. Mitochondrial dysfunction has been widely observed under pathological conditions. The decline of mitochondrial quality is proposed as one of the driving forces of ageing and ageing-related degenerative diseases. Working with yeast (Saccharomyces cerevisiae), mammalian cell lines, and genetically-modified mice, we aim to uncover evolutionarily conserved mechanisms surveying and maintaining mitochondrial quality.
Mitochondrial outer-membrane (MOM) harbors protein machineries essential for protein import, fusion/fission dynamics, and other signaling and metabolic functions. The quality control pathways of MOM proteome remain poorly characterized. Using yeast as the model organism, we combine genetic and biochemical approaches to identify key players of MOM protein quality control and their biochemical mechanisms.
Mitochondrial fusion/fission dynamics are essential for mitochondrial function. Mutations of mitochondrial dynamics regulators (including OPA1, Mfn2, and Drp1) cause severe neuronal and muscular degenerative disorders. Mitochondrial over-fission has been widely associated with sporadic and familiar degenerative diseases. We aim to develop small molecules regulating mitochondria dynamics and explore their application in disease models.
More than 99% of the mitochondrial proteins are encoded by nuclear genes and expressed in cytoplasm. The intimate communication between mitochondria and its environment is critical for maintaining mitochondrial homeostasis. We aim to reveal the cellular adaptive responses upon mitochondrial dysfunction, and their potential applications in diseases.




发表文章
Publication
1. Wu X, Li LL, Jiang H. (2018). Mitochondrial inner-membrane proteaseYme1degrades outer-membrane proteinsTom22and Om45. J Cell Biol. 2018 Jan 2;217(1):139-149.
2. Wu X, Li LL, Jiang H. (2016). Doa1 targets ubiquitinated substrates for mitochondria-associated degradation. J Cell Biol. 2016 Apr 11;213(1):49-63. (Commented by J Cell Biol. 2016 Apr 11;213(1):7-9.)
3. Jiang X, Li L, Ying Z, Pan C, Huang S, Li L, Dai M, Yan B, Li M, Jiang H, Chen S, Zhang Z, Wang X (2016). A Small Molecule That Protects the Integrity of the Electron Transfer Chain Blocks the Mitochondrial Apoptotic Pathway. Mol Cell. 2016 Jul 21;63(2):229-39.
4. Jiang X, Jiang H, Shen Z, Wang X. (2014). Activation of mitochondrial protease OMA1 by Bax and Bak promotes cytochrome c release during apoptosis. Proc Natl Acad Sci U S A. 2014 Oct 14;111(41):14782-7.
5. Wang Z, Jiang H, Chen S, Du F, Wang X. (2012). The mitochondrial phosphatase PGAM5 functions at the convergence point of multiple necrotic death pathways. Cell. 2012 Jan 20;148(1-2):228-43.
6. Guo W, Jiang H, Gray V, Dedhar S, Rao Y (2007). Role of the integrin-linked kinase (ILK) in determining neuronal polarity. Dev Biol. 306:457-68.
7. Ward ME, Jiang H, Rao Y (2005). Regulated formation and selection of neuronal processes underlie directional guidance of neuronal migration. Mol Cell Neurosci 30:378-87.
8. Jiang H, Rao Y (2005). Axon formation: fate versus growth. Nat Neurosci. 8:544-6.
9. Jiang H, Guo W, Liang X, Rao Y (2005). Both the establishment and the maintenance of neuronal polarity require active mechanisms: critical roles of GSK-3beta and its upstream regulators. Cell 120:123-35. (Highlighted by Science, Nature Review Neuroscience, and Current Biology)