Mingyao Ying, PhD

Johns Hopkins Affiliations:

Johns Hopkins School of Medicine Faculty

Languages

English

Gender

Male

About Mingyao Ying

Primary Academic Title

Associate Professor of Neurology

Background

Dr. Ying received his Ph.D. degree from Fudan University in China for research on neurodegenerative diseases. He completed post-doctoral research on Parkinson’s disease with Dr. Ted Dawson at the Johns Hopkins University School of Medicine, and most recently on transcriptional regulation of brain tumor stem cells with Dr. John Laterra at the Kennedy Krieger Institute.

Research Interests

Identifying new targets that regulate the self-renewal and differentiation of normal and malignant stem cells.

Research Summary

Dr. Ying received his scientific training in the field of neurodegenerative diseases and brain tumors. His research focuses on identifying new targets that regulate the self-renewal and differentiation of normal and malignant stem cells. He was first to show that mutant transcription factor, atrophin-1, induces transcription deregulation and neurodegenerative phenotypes in a mouse model of dentatorubral-pallidoluysian atrophy, which can be ameliorated by histone deacetylase inhibitor. As a postdoctoral fellow in Johns Hopkins School of Medicine, Dr. Ying studied the molecular mechanism of neurodegenerative diseases and established a new mouse model of Parkinson’s disease.

After joining the neuro-oncology laboratory in Kennedy Krieger Research Institute, Dr. Ying has increasingly focused on the functions of multiple transcription factors in human brain tumor stem cells. His published research identifies a novel transcription factor, Krupple-like factor 9, which can differentiate brain tumor stem cells, inhibit their tumor propagation, and inhibit notch signaling in these cells. He has developed a transcription-factor-based differentiation strategy for efficiently generating functional and transplantable dopaminergic neurons from human pluripotent stem cells. Dr. Ying is currently engaged in identifying transcription factors with potential applications in regenerative medicine and cancer therapeutics.

Selected Publications

1. Ying M, Tilghman J, Wei Y, Guerrero-Cazares H, Quinones-Hinojosa A, Ji H, Laterra J. KLF9 Inhibits Glioblastoma Stemness through Global Transcription Repression and Integrin-α6 Inhibition. J Biol Chem. 2014 Oct 6. pii: jbc.M114.588988. [Epub ahead of print]
1. Jonathan Sagal, Xiping Zhan, Jinchong Xu, Jessica Tilghman, Senthilkumar S. Karuppagounder, Li Chen, Valina L. Dawson, Ted M. Dawson, John Laterra and Mingyao Ying. Proneural Transcription Factor Atoh1 Drives Highly Efficient Differentiation of Human Pluripotent Stem Cells into Dopaminergic Neurons. Stem Cells Transl Med. 2014 Aug;3(8):888-98.
1. Jessica Tilghman, Hao Wu, Yingying Sang, Xiaohai Shi, Hugo Guerrero-Cazares, Alfredo Quinones-Hinojosa, Charles G. Eberhart, John Laterra and Mingyao Ying. HMMR maintains the stemness and tumorigenicity of glioblastoma stem-like cells. Cancer Res. 2014 Jun 1;74(11):3168-79.
1. Yunqing Li, Angela Li, Martin Glas, Bachchu Lal, Mingyao Ying, Yingying Sang, Shuli Xia, Daniel Trageser, Hugo Guerrero-Cázares, Charles G. Eberhart, Alfredo Quiñones-Hinojosa, Bjorn Scheffler, and John Laterra c-Met signaling induces a reprogramming network and supports the glioblastoma stem-like phenotype. Proc Natl Acad Sci U S A. 2011 Jun 14;108(24):9951-6.
1. Mingyao Ying*, Shervin Wang*, Yingying Sang, Peng Sun, C. Rory Goodwin, Alfredo Quinones-Hinojosa, Bachchu Lal, John Laterra and Shuli Xia. Regulation of glioblastoma stem cells by retinoic acid: role for Notch pathway inhibition. Oncogene. 2011 Aug 4;30(31):3454-67. (*: contributed equally)
1. Mingyao Ying, Yingying Sang, Yunqing Li, Hugo Guerrero-Cazares, Alfredo Quinones-Hinojosa, Angelo L. Vescovi, Charles G. Eberhart, Shuli Xia, John Laterra. KLF9, a differentiation-associated transcription factor, suppresses Notch1 signaling and inhibits glioblastoma-initiating stem cells. Stem Cells. 2011 Jan; 29(1):20-31. [Highlighted on the cover]
1. Yu J, Ying M, Zhuang Y, Xu T, Han M, Wu X, Xu R. C-terminal deletion of the atrophin-1 protein results in growth retardation but not neurodegeneration in mice. Dev Dyn. 2009 Aug 13;238(10):2471-2478.
1. Daher JP*, Ying M*, Banerjee R, McDonald RS, Hahn MD, Yang L, Flint Beal M, Thomas B, Dawson VL, Dawson TM, Moore DJ. Conditional transgenic mice expressing C-terminally truncated human alpha-synuclein (alphaSyn119) exhibit reduced striatal dopamine without loss of nigrostriatal pathway dopaminergic neurons. Molecular Neurodegeneration. 2009 Jul 24;4:34. (*: contributed equally)
1. Ying M, Xu R, Wu X, Zhu H, Zhuang Y, Han M, Xu T. Sodium butyrate ameliorates histone hypoacetylation and neurodegenerative phenotypes in a mouse model for DRPLA. J Biol Chem. 2006 May 5;281(18):12580-6.