Area of research
Molecular Biology · Cellular and Molecular Neuroscience
Research interest
Research interests include Genetic Neurodegenerative Diseases, Mitochondrial Function and Pathology, Muscle Physiology and Disorders, and Neurological disorders and treatments.
In vivo self-assembled siRNAs ameliorate neurological pathology in TDP-43-associated neurodegenerative disease.
Primate abnormal spindle-like microcephaly-associated knockout causes severe microcephaly and oligodendrocyte loss in the brain.
Single-nucleus transcriptomics of an engineered pig model reveals microglia-T cell interactions driving Huntington's disease neurodegeneration.
MANF is essential for astrocyte survival in the monkey brain.
Precise excision of expanded GGC repeats in NOTCH2NLC via CRISPR/Cas9 for treating neuronal intranuclear inclusion disease.
Reduced mesencephalic astrocyte-derived neurotrophic factor expression by mutant androgen receptor contributes to neurodegeneration in a model of spinal and bulbar muscular atrophy pathology.
The role of oligodendroglial dysfunction in Huntington's disease.
TRIM37 is a primate-specific E3 ligase for Huntingtin and accounts for the striatal degeneration in Huntington's disease.
HAP40 modulates mutant Huntingtin aggregation and toxicity in Huntington’s disease mice
HAP40 modulates mutant Huntingtin aggregation and toxicity in Huntington's disease mice.
CHD8 mutations increase gliogenesis to enlarge brain size in the nonhuman primate.
A Specific Mini-Intrabody Mediates Lysosome Degradation of Mutant Huntingtin.
Neuropathological insights from SHANK3 mutant animal models
Animal models for research on neurodegenerative diseases
PINK1 kinase dysfunction triggers neurodegeneration in the primate brain without impacting mitochondrial homeostasis.
Differential expression and roles of Huntingtin and Huntingtin-associated protein 1 in the mouse and primate brains.
AHI1: linking depression and impaired antiviral immune response.
Ahi1 regulates the nuclear translocation of glucocorticoid receptor to modulate stress response.
Accumulation of Endogenous Mutant Huntingtin in Astrocytes Exacerbates Neuropathology of Huntington Disease in Mice.
Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form
Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form.
Loss of Hap1 selectively promotes striatal degeneration in Huntington disease mice
Cerebellum-enriched protein INPP5A contributes to selective neuropathology in mouse model of spinocerebellar ataxias type 17
Lack of RAN-mediated toxicity in Huntington’s disease knock-in mice
Phosphorylation of myelin regulatory factor by PRKG2 mediates demyelination in Huntington's disease
Author Correction: Truncation of mutant huntingtin in knock-in mice demonstrates exon1 huntingtin is a key pathogenic form.
Maternal valproic acid exposure leads to neurogenesis defects and autism-like behaviors in non-human primates
CRISPR/Cas9-mediated PINK1 deletion leads to neurodegeneration in rhesus monkeys
Caspase-4 mediates cytoplasmic accumulation of TDP-43 in the primate brains
A CRISPR monkey model unravels a unique function of PINK1 in primate brains