Parkinson disease (PD) is the most common neurodegenerative movement disorder. Although L-DOPA treatment is applied to alleviate motor deficit in PD patients, there is no cure which can halt or slow the progressive and rather ive loss of dopaminergic neurons.
Our lab has focused on understanding molecular mechanisms of cell death execution in PD pathogenesis. We are particularly interested in poly (ADP-ribose) dependent cell death pathways and its interaction with PD-associated disease proteins. Advanced genetic tools are used to invent PD mouse and cell models to study underlying molecular mechanisms of dopaminergic cell loss. For example, conditional toxic protein expression are temporally and spatially controlled by using Tet-Off conditional genetic switch. In case of genetic ablation study, CRISPR-cas9 system has been applied to intervene specific genetic component in the pathway of cell degeneration.
Another research topic includes identification of a-synuclein membrane receptors which can mediate pathology propagation. a-synuclein pathology oftentimes spreads from one brain region to another, therefore identification of a-synuclein receptors holds important therapeutic value in preventing progression of PD pathogenesis.
1. Ham S et al. Amyloid-like oligomerization of AIMP2 contributes to α-synuclein interaction and Lewy-like inclusion. Sci Transl Med. 2020 Nov 1112(569) (Corresponding)
2. Kim H et al. Quantitative analysis of nasal transcripts reveals potential biomarkers for Parkinsons disease. Sci Rep. 2019 Jul 319(1) (Corresponding)
3. Kim H et al. Rhododendrin-Induced RNF146 Expression via Estrogen Receptor β Activation is Cytoprotective Against 6-OHDA-Induced Oxidative Stress. Int J Mol Sci. 2019 Apr 1020(7). (Corresponding)
4. Yun SP et al. α-Synuclein accumulation and GBA deficiency due to L444P GBA mutation contributes to MPTP-induced parkinsonism. Mol Neurodegener. 2018 Jan 813(1) (Corresponding)
5. Kim H et al. CRISPR-Cas9 Mediated Telomere Removal Leads to Mitochondrial Stress and Protein Aggregation. Int J Mol Sci. 2017 Oct 318(10) (Corresponding)