Liping Wang

About

The goal of my research is to unravel the role of lipid metabolism underlying the pathological mechanisms of human neurodegenerative diseases by taking advantage of sophisticated and versatile technologies in genetic, molecular biology, cellular biology, and biochemistry in model organisms and tissue cultures. Through a detailed investigation of the pathology of neurological disorders at molecular levels, we can discover specific targets for drug development and treatment.
I am currently a graduate student in Dr. Hugo Bellen’s lab at Baylor College of Medicine. My project focus on understanding the roles of sphingolipid metabolism in the pathogenesis of lysosomal storage diseases as well as neurodegenerative diseases including Gaucher Disease (GD), Parkinson Disease (PD), and Infantile Neuroaxonal Dystrophy (INAD). The gene I am interested in is GBA1, of which homozygous variants cause GD and heterozygous variants show a significantly high risk for developing PD. Moreover, my data indicate some striking similarities between the molecular pathogenesis of INAD and GD. I use Drosophila Melanogaster, the commonly used and the most powerful model organism in genetics, to study the defects associated with loss of GBA1. The mechanisms we identified in flies are evolutionarily conserved as it is confirmed in the mammalian cell lines. I discover a novel and cell non-autonomous role of sphingolipid metabolism in the pathogenesis of neurological disorders by investigating the molecular and cellular mechanisms that underlie the phenotypes caused by loss of GBA1. These findings may point out some pathologies that were neglected in clinics regarding neurodegenerative diseases, which may further shed light on novel drug development.

Employment

• University of Southern California Resource Employee
  2016 - Present

Education

• Baylor College of Medicine PhD
  2017 - Present
• University of Southern California MS
  2014 - 2016

Projects & Funding

Projects & funding information is unavailable.

Publications (4)

• Retromer subunit, VPS29, regulates synaptic transmission and is required for endolysosomal function in the aging brain.
  eLife 2020 DOI: 10.7554/elife.51977
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• Sphingolipids in the Pathogenesis of Parkinson's Disease and Parkinsonism.
  Trends in endocrinology and metabolism: TEM 2018 DOI: 10.1016/j.tem.2018.11.003
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• Phospholipase PLA2G6, a Parkinsonism-Associated Gene, Affects Vps26 and Vps35, Retromer Function, and Ceramide Levels, Similar to α-Synuclein Gain.
  Cell metabolism 2018 DOI: 10.1016/j.cmet.2018.05.019
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• Phosphorylation of Synaptojanin Differentially Regulates Endocytosis of Functionally Distinct Synaptic Vesicle Pools.
  The Journal of neuroscience : the official journal of the Society for Neuroscience 2016 DOI: 10.1523/jneurosci.1470-16.2016
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