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Minghui Gao
Publisher:高雪  Time2017-09-28 View:175

Minghui Gao
Phone: 86-451-86402027
Research Area: programmed cell death, autophagy, cancer metabolism

Dr. Minghui Gao received his PhD degree atNational Institute of Biological Sciences, Beijing & China Agricultural University in Chinain 2009, and then Dr. Gao joined Xuejun Jiang Lab at Memorial Sloan-Kettering Cancer Center in New York for his postdoctoral training. During his postdoc training, Dr. Gao mainly focused on the mechanism of programmed cell death and its implication in human diseases. Dr. Gao will join the HIT Center for Life Sciences & the School of Life Sciences and Technology of the Harbin Institute of Technology in January 2018.


Research Interests

     Death is the common fate of all living matters, including every cell in our bodies. While often detrimental and a sign of deterioration, cell death can also be an integral part of life and be harnessed, or programmed, to benefit the multicellular organism – the concept of “programmed cell death”. Programmed cell death plays critical roles in development and tissue homeostasis of multicellular organisms, and malfunction of programmed cell death contributes to the pathogenesis of a variety of human diseases, including cancer. We employ multiple approaches to study the molecular basis of programmed cell death. We also seek to translate our basic research findings into novel cancer therapies.

Currently, we focus on three topics:

1.Understand the molecular basis of ferroptosis and its function in human diseases

Ferroptosis is an iron-dependent form of regulated necrosis. Mechanistically, ferroptosis is distinct from apoptosis and other regulated necrosis, and is dependent on cellular iron (thus the name) and reactive oxygen species (ROS). Although ferroptosisis strongly implicated in human diseases, currently theprecise molecular mechanisms and biological functions of ferroptosisremain poorly understood. It is thus important to understand the molecular basis of ferroptosis, as such knowledge can help to predict the therapeutic value of inducing ferroptosis in cancer treatment and provide possibilities for inhibition of this form of cell death in pathologically relevant scenarios (such as ischemia-reperfusion induced organism injury).

2.Study the molecular function of autophagy in programmed cell death

Autophagy is a conserved intracellular catabolic process that delivers cellular components to the lysosome for degradation. The role of autophagy in cell death and cell survival has been controversial. It is well accepted that under most biological conditions autophagy functions as a pro-survival mechanism. On the other hand, autophagy may also be a cell death mechanism under certain specific contexts — the so-called ‘autophagic cell death’, via yet to be defined mechanisms. We are interested in investigating the molecular function of autophagy in programmed cell death.  

3.Investigate cancer cell metabolism

Onehallmark of tumor cell is the ability to acquire necessary nutrients from a frequently nutrient-poor environment and utilize these nutrients to maintain viability and build new biomass. Our interest in cancer metabolism is to investigate the regulation mechanism of amino acids metabolism in tumor, precisely how amino acids metabolism becomes reprogrammed in cancer cells in response to tumor microenvironment stress and how to exploit metabolic changes for therapeutic benefit.


Techniques and Tools in the Lab

We use multi-disciplinary approaches including cell biology, biochemistry, bioinformatics and mouse genetics in our studies.


Selected Publications

  1. Gao  M*#,  Yi J* Zhu J, Minikes A, Monian P, Thompson C, and Jiang X#.Role  of Mitochondria in Ferroptosis.Molecular  Cell.2018.73, 1–10.(IF:14.248)

  2. Gao  M#,  Jiang X#.To Eat or Not to Eat – The Metabolic Flavor of  Ferroptosis.Current Opinion in Cell Biology.2018  51:58-64(IF:10.015)

  3. Gao M#, Monian P, Pan Q, Wei Zhang W, Xiang J, Jiang X#.Ferroptosis is an autophagic cell death process.Cell Research 2016 26(9):1021-32 (#Co-corresponding authors,IF: 15.606, Citation: 28)

  4. Gao M, Monian P, Jiang X. Metabolism and Iron Signaling in Ferroptotic Cell Death.Oncotarget 2015 6(34):35145-6. (IF: 5.168, Citation: 3)

  5. Gao M, Monian P, Quadri N, Ramasamy R, Jiang X. Glutaminolysis and Transferrin Regulate Ferroptosis.Molecular Cell. 2015 59(2):298-308. (IF: 14.714, Citation: 56)

  6. Gao M, Wang X, Wang D, Xu F, Ding X, Zhang Z, Bi D, Cheng YT, Chen S, Li X, Zhang Y. Regulation of cell death and innate immunity by two receptor-like kinases in Arabidopsis.Cell Host & Microbe(2009) 6: 34-44 (highlighted byNature China,IF: 14.946, Citation: 200)

  7. Gao M*, Liu J*, Bi D, Zhang Z, Cheng F, Chen S, Zhang Y. MEKK1, MKK1/MKK2 and MPK4 function together in a mitogen-activated protein kinase cascade to regulate innate immunity in plants.Cell Research(2008)18:1190–1198 (* co-first authors) (Cover Story) (IF: 15.606, Citation: 218)

  8. Zhang Z, Liu Y, Huang H,Gao M, Wu D, Kong Q, and Zhang Y. Sensing the disruption of a MAP kinase cascade by an NLR protein through a MAP kinase substrate. EMBO Reports 16 December 2016, online(IF: 8.568, Citation: 2)

  9. Bradbury M, Kim S, Zhang L, Ma K, Riegman M, Chen F, Ingold I, Conrad M, Turker M,Gao M, Jiang X, Monette S, Mohan P, Gonen M, Zanzonico P, Quinn T, Wiesner U, Overholtzer M. Ultrasmall Nanoparticles Induce Ferroptosis of Nutrient-Deprived Cancer Cells and Suppress Tumor Growth.Nature Nanotechnology 2016(IF: 38.986, Citation: 27)

  10. Sun T, Zhang Q,Gao M, Zhang Y.Regulation of SOBIR1 accumulation and activation of defense responses in bir1-1 by specific components of ER quality control.ThePlant Journal. 2014 77 (5):748-56. (IF: 5.901, Citation: 14)

  11. Kong Q*, Qu N*,Gao M, Zhang Z, Ding X, Yang F, Li Y, Dong OX, Chen S, Li X, Zhang Y. The MEKK1-MKK1/MKK2-MPK4 kinase cascade negatively regulates immunity mediated by a mitogen-activated protein kinase kinasekinase in Arabidopsis.Plant Cell. 2012 (5):2225-36. (* co-first authors) (IF: 8.688, Citation: 96)

  12. Zhang Z, Wu Y,Gao M, Zhang J, Kong Q, Liu Y, Ba H, Zhou J, Zhang Y. Disruption of PAMP-induced MAP kinase cascade by a Pseudomonas syringae effector activates plant immunity mediated by the NB-LRR protein SUMM2.Cell Host Microbe.2012 (3):253-63. (IF: 14.946, Citation: 147)

  13. Zhang, Y., Xu, S., Ding, P., Wang, D., Cheng, Y., He, J.,Gao, M.,Xu, F., Li, Y., Zhu, Z., Li, X., and Zhang, Y.2010. Control of salicylic acid synthesis and systemic acquired resistance by two members of a plant-specific family of transcription factors.Proceedings of the National Academy of Sciences(track II).107(42):18220-18225. (IF: 9.661, Citation: 117)

  14. Zhang J, Li W, Xiang T, Liu Z, Laluk K, Ding X, Zou Y,Gao M, Zhang X, Chen S, Mengiste T, Zhang Y, Zhou JM. Receptor-like cytoplasmic kinases integrate signaling from multiple plant immune receptors and are targeted by aPseudomonas.syringae.effector.Cell Host &Microbe, 2010 (4):290-301. (highlighted byCell Host & Microbe,2010) . (IF: 14.946, Citation: 384)

  15. Monaghan J, Xu F,Gao M, Zhao Q, Palma K, Long C, Chen S, Zhang Y, Li X. Two Prp19-Like U-Box Proteins in the MOS4-Associated Complex Play Redundant Roles in Plant Innate Immunity.PLoSPathog5(7): e1000526 (IF: 7.003, Citation:80)