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Minghui Gao
Publisher:高雪  Time2017-09-14 View:230

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)