蒋辉 博士

北京生命科学研究所高级研究员

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

Phone: 010-80726688-8620

Email: jianghui@nibs.ac.cn

教育经历

Education

2008   博士，中科院上海生命科学研究院神经所
Ph.D.  Institute of Neuroscience, Shanghai Institute of Biological Sciences, Chinese Academy of Sciences
2001   学士，南京大学生物化学系
BS. Biochemistry, Nanjing University, China

工作经历

Professional Experience

2016-       高级研究员，北京生命科学研究所
Associate Investigator, National Institute of Biological Sciences, Beijing, China
2011-2016   NIBS fellow, 北京生命科学研究所
NIBS Fellow, National Institute of Biological Sciences, Beijing, China
2008-2011   博士后，德克萨斯大学西南医学中心王晓东实验室

Postdoctoral research with Dr. Xiaodong Wang, UT-Southwestern, USA

研究概述

Research Description

线粒体是负责能量供应的细胞器，也是细胞凋亡的关键执行者和炎症反应的重要参与者。线粒体功能紊乱和损伤积累是衰老和衰老相关疾病发生的重要诱因之一。我们实验室专注于理解线粒体质量控制和稳态维持机制，以及这些机制在退行性疾病和衰老中的作用。我们利用酵母,细胞,小鼠等模型,整合遗传,生化,化学生物学等手段,研究以下重要问题: 1. 线粒体质量控制体系,包括蛋白质质量控制和线粒体自噬,的分子机理及其生物学功能。2.线粒体疾病,尤其是呼吸链损伤相关神经退行性疾病,的致病机理及治疗靶点开发。3.线粒体损伤与慢性炎症和退行性病变的相互关系。

Mitochondrion is the powerhouse of the cell and a key player in apoptosis and inflammation. Mitochondrial dysfunction is a driving force of aging and aging-related degenerative diseases. We exploit yeast, cultured cell, and mouse models to uncover mechanisms surveying mitochondrial quality and maintaining mitochondrial homeostasis. We focus on the following questions: 1. mitochondrial quality control mechanisms, including protein quality control and mitophagy; 2. the pathological mechanisms and therapeutic targets for mitochondrial diseases; 3. the relationship between mitochondrial damage, chronic inflammation, and degenerative diseases.

发表文章

Publication

1. Liu S, Fu S, Wang G, Cao Y, Li L, Li X, Yang J, Li N, Shan Y, Cao Y, Ma Y, Dong MQ, Liu Q, Jiang H. Glycerol-3-phosphate biosynthesis regenerates cytosolic NAD⁺ to alleviate mitochondrial diseases. Cell Metabolism 2021 Oct 5; 33, 1-14.

2. Liu S, Liu S, He B, Li L, Li L, Wang J, Cai T, Chen S, Jiang H. OXPHOS deficiency activates global adaptation pathways to maintain mitochondrial membrane potential. EMBO Rep. 2021 Apr 7; 22(4):e51606.

3. Jiang H. Quality control pathways of tail-anchored proteins. BBA Mol Cell Res. 2021 Feb;1868(2):118922. (review)

4. Zheng J, Li L, Jiang H. Molecular pathways of mitochondrial outer membrane protein degradation. Biochem Soc Trans. 2019 Oct 31; 47(5):1437-1447. (review)

5. Li L^#, Zheng J^#, Wu X*, Jiang H*. Mitochondrial AAA-ATPase Msp1 detects mislocalized tail-anchored proteins through a dual-recognition mechanism. EMBO Rep. 2019 Apr; 20(4). pii: e46989.

6. Wu X*, Li LL, Jiang H*. (2018). Mitochondrial inner-membrane protease Yme1 degrades outer-membrane proteins Tom22 and Om45. J Cell Biol. 2018 Jan 2; 217(1):139-149.

7. 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. (Highlighted by J Cell Biol. 2016 Apr 11;213 (1):7-9.)

8. 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.

9. 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.

10. 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.

11. 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.

12. 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.

13. Jiang H, Rao Y (2005). Axon formation: fate versus growth. Nat Neurosci. 8:544-6.

14. 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)
# co-first author, * co-corresponding author.