Michael K. Lee

Accumulation of proteolytic fragments of mutant presenilin 1 and accelerated amyloid deposition are co-regulated in transgenic mice.

Human alpha-synuclein-harboring familial Parkinson's disease-linked Ala-53 --> Thr mutation causes neurodegenerative disease with alpha-synuclein aggregation in transgenic mice.

No-reflow is an independent predictor of death and myocardial infarction after percutaneous coronary intervention.

Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase.

Axonal transport of human alpha-synuclein slows with aging but is not affected by familial Parkinson's disease-linked mutations.

Stabilization of alpha-synuclein protein with aging and familial parkinson's disease-linked A53T mutation.

Association of DJ-1 and parkin mediated by pathogenic DJ-1 mutations and oxidative stress.

Aggregation promoting C-terminal truncation of alpha-synuclein is a normal cellular process and is enhanced by the familial Parkinson's disease-linked mutations.

Abeta deposition is associated with enhanced cortical alpha-synuclein lesions in Lewy body diseases.

Antiapoptotic property of human alpha-synuclein in neuronal cell lines is associated with the inhibition of caspase-3 but not caspase-9 activity.

Alpha-synuclein phosphorylation enhances eosinophilic cytoplasmic inclusion formation in SH-SY5Y cells.

Locomotor hyperactivity and alterations in dopamine neurotransmission are associated with overexpression of A53T mutant human alpha-synuclein in mice.

Ruptured left gastric artery aneurysm: unique presentation with hemothorax and hemomediastinum.

Parkinson's disease alpha-synuclein transgenic mice develop neuronal mitochondrial degeneration and cell death.

Ubiquitin-proteasome system stress sensitizes ovarian cancer to proteasome inhibitor-induced apoptosis.

Inclusion body formation and neurodegeneration are parkin independent in a mouse model of alpha-synucleinopathy.

Wild-type and mutant alpha-synuclein induce a multi-component gene expression profile consistent with shared pathophysiology in different transgenic mouse models of PD.

Differential regulation of small heat shock proteins in transgenic mouse models of neurodegenerative diseases.

Myosin II co-chaperone general cell UNC-45 overexpression is associated with ovarian cancer, rapid proliferation, and motility.

Lysine 63-linked ubiquitination promotes the formation and autophagic clearance of protein inclusions associated with neurodegenerative diseases.

Ubiquitin proteasome system stress underlies synergistic killing of ovarian cancer cells by bortezomib and a novel HDAC6 inhibitor.

Amyloid pathology is associated with progressive monoaminergic neurodegeneration in a transgenic mouse model of Alzheimer's disease.

Increased expression of alpha-synuclein reduces neurotransmitter release by inhibiting synaptic vesicle reclustering after endocytosis.

Synphilin-1 attenuates neuronal degeneration in the A53T alpha-synuclein transgenic mouse model.

Passive (amyloid-β) immunotherapy attenuates monoaminergic axonal degeneration in the AβPPswe/PS1dE9 mice.

Resistance to MPTP-neurotoxicity in α-synuclein knockout mice is complemented by human α-synuclein and associated with increased β-synuclein and Akt activation.

Dopaminergic neuronal loss, reduced neurite complexity and autophagic abnormalities in transgenic mice expressing G2019S mutant LRRK2.

Magnetization transfer and adiabatic R 1ρ MRI in the brainstem of Parkinson's disease.

Neurodegenerative phenotypes in an A53T α-synuclein transgenic mouse model are independent of LRRK2.

Accumulation of toxic α-synuclein oligomer within endoplasmic reticulum occurs in α-synucleinopathy in vivo.

Endoplasmic reticulum stress is important for the manifestations of α-synucleinopathy in vivo.

Small-molecule RA-9 inhibits proteasome-associated DUBs and ovarian cancer in vitro and in vivo via exacerbating unfolded protein responses.