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Yulan Xiong, Ph.D.Assistant Professor of Neuroscience
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| Degree | Institution | Major |
|---|---|---|
| Ph.D. | Lancaster University, UK | Biochemistry & Molecular Genetics |
Post-Graduate Training
| Training | Institution | Specialty |
|---|---|---|
| Postdoctoral | Johns Hopkins University School of Medicine | Neurology |
Awards
| Name of Award/Honor | Awarding Organization |
|---|---|
| NIH R01 Grant (2019-2024) | NIH/NINDS |
| Stanley Fahn Junior Faculty Award (2019-2022) | Parkinson's Foundation |
| C-NAP COBRE Center Pilot Grant | NIH/NIGMS |
| Research Grant (2017-2018) | American Parkinson's Disease Association (APDA) |
| K-INBRE Bridging Award | NIH/NIGMS |
| Success for Young Investigators SUCCESS-FYI Award (2016, 2017, 2018) | KSU-CVM |
| Innovative Research Awards | Johnson Center for Basic Cancer Research |
| The William N. & Bernice E. Bumpus Foundation Innovation Awards (2015-2018) | The William N. & Bernice E. Bumpus Foundation |
| K01 Mentored Research Scientist Development Award (2014-2022) | NIH/NIA |
| Rapid Response Innovation Awards | The Michael J. Fox foundation (MJFF) |
| Postdoctoral Fellowship Award | American Parkinson’s Disease Association (APDA) |
Molecular Pathophysiology of Parkinson's disease
Our lab focuses on understanding the molecular mechanisms underlying neurodegenerative diseases, with a specific emphasis on Parkinson’s disease (PD).
Parkinson’s disease (PD) is the most common movement disorder and the second most common neurodegenerative disorder after Alzheimer’s disease. Currently there is no effective therapy. The Xiong lab aims to understand the mechanisms underlying PD with a specific focus on four major questions: 1) How do PD-associated proteins contribute to dopaminergic neurodegeneration? 2) What are the new molecules and how are they involved in PD pathogenesis? 3) What is the human relevance of our findings? 4) How to develop the pharmacological strategies to slow down the PD symptoms?
To answer these questions, Dr. Xiong’s group has developed a variety of model systems from single cell organism budding yeast to Drosophila, mice, primary and human neuronal cultures. Using these systems, the lab’s general approaches are to use a powerful combination of genetics, molecular biology, viral approaches and behavioral analysis to decipher the molecular mechanisms underlying neurodegenerative diseases in human. The lab’s research goal is to identify molecular therapeutic targets that will ultimately lead to developing effective biomarkers and treatments for PD.
The Xiong lab welcomes motivated postdocs and graduate students to join the team.
Accepting Lab Rotation Students: Summer 2022, Fall 2022, and Spring 2023
Journal Articles
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Dysregulated mRNA Translation in the G2019S LRRK2 and LRRK2 Knock-Out Mouse Brains.
eNeuro 2021 Nov;8(6):
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Dysregulation of the AP2M1 phosphorylation cycle by LRRK2 impairs endocytosis and leads to dopaminergic neurodegeneration.
Science signaling 2021 Jul;14(693):
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Complement and Coagulation Cascades are Potentially Involved in Dopaminergic Neurodegeneration in α-Synuclein-Based Mouse Models of Parkinson's Disease.
Journal of proteome research 2021 Jul;20(7):3428-3443
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LRRK2 Modulates the Exocyst Complex Assembly by Interacting with Sec8.
Cells 2021 Jan;10(2):
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PARIS induced defects in mitochondrial biogenesis drive dopamine neuron loss under conditions of parkin or PINK1 deficiency.
Molecular neurodegeneration 2020 Mar;15(1):17
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In vivo methylation of OLA1 revealed by activity-based target profiling of NTMT1.
Chemical science 2019 Sep;10(35):8094-8099
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Headcase and Unkempt Regulate Tissue Growth and Cell Cycle Progression in Response to Nutrient Restriction.
Cell reports 2019 Jan;26(3):733-747.e3
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Robust kinase- and age-dependent dopaminergic and norepinephrine neurodegeneration in LRRK2 G2019S transgenic mice.
Proceedings of the National Academy of Sciences of the United States of America 2018 Feb;115(7):1635-1640
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Overexpression of Parkinson's Disease-Associated Mutation LRRK2 G2019S in Mouse Forebrain Induces Behavioral Deficits and α-Synuclein Pathology.
eNeuro 2017 Mar;4(2):
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LRRK2 G2019S transgenic mice display increased susceptibility to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mediated neurotoxicity.
Journal of chemical neuroanatomy 2016 Oct;76(Pt B):90-97
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Pathological α-synuclein transmission initiated by binding lymphocyte-activation gene 3.
Science (New York, N.Y.) 2016 Sep;353(6307):
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Functional interaction of Parkinson's disease-associated LRRK2 with members of the dynamin GTPase superfamily.
Human molecular genetics 2014 Apr;23(8):2055-77
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Ribosomal protein s15 phosphorylation mediates LRRK2 neurodegeneration in Parkinson's disease.
Cell 2014 Apr;157(2):472-485
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LRRK2 affects vesicle trafficking, neurotransmitter extracellular level and membrane receptor localization.
PloS one 2013 Jan;8(10):e77198
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ArfGAP1 is a GTPase activating protein for LRRK2: reciprocal regulation of ArfGAP1 by LRRK2.
The Journal of neuroscience : the official journal of the Society for Neuroscience 2012 Mar;32(11):3877-86
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Transcriptional responses to loss or gain of function of the leucine-rich repeat kinase 2 (LRRK2) gene uncover biological processes modulated by LRRK2 activity.
Human molecular genetics 2012 Jan;21(1):163-74
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The AAA+ ATPase Thorase regulates AMPA receptor-dependent synaptic plasticity and behavior.
Cell 2011 Apr;145(2):284-99
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Reevaluation of phosphorylation sites in the Parkinson disease-associated leucine-rich repeat kinase 2.
The Journal of biological chemistry 2010 Sep;285(38):29569-76
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GTPase activity plays a key role in the pathobiology of LRRK2.
PLoS genetics 2010 Apr;6(4):e1000902
Book Chapters
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Linking the leucine-rich repeat kinase 2 (LRRK2) gene, animal models and Parkinson’s disease.
The Neuroscience of Parkinson’s disease: Volume 2: Genetics, Neurology, Behavior, and Diet in Parkinson's Disease 2020 Aug;
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Models of LRRK2-Associated Parkinson's Disease.
Advances in neurobiology 2017 Jan;163-191
Reviews
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Modeling Parkinson's Disease in Drosophila: What Have We Learned for Dominant Traits?
Frontiers in neurology 2018 Jan;9228
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LRRK2 GTPase dysfunction in the pathogenesis of Parkinson's disease.
Biochemical Society transactions 2012 Oct;40(5):1074-9