M
Michael K. Lee
Researcher at University of Minnesota
Publications - 143
Citations - 40211
Michael K. Lee is an academic researcher from University of Minnesota. The author has contributed to research in topics: Presenilin & Neurodegeneration. The author has an hindex of 71, co-authored 136 publications receiving 38151 citations. Previous affiliations of Michael K. Lee include University of Virginia & Johns Hopkins University.
Papers
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Nucleotide sequence of the chromosome 14-encoded S182 cDNA and revised secondary structure prediction
TL;DR: The Nucleotide sequence of the chromosome 14-encoded S182 cDNA and revised secondary structure prediction was presented in this paper. But the secondary structure was not discussed. But the results were similar to those presented in this paper.
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Cp/Heph mutant mice have iron-induced neurodegeneration diminished by deferiprone.
L. Zhao,L. Zhao,Majda Hadziahmetovic,Majda Hadziahmetovic,Chenguang Wang,Chenguang Wang,Xueying Xu,Ying Song,Hyder A. Jinnah,Jolanta Wodzinska,Jared Iacovelli,Natalie Wolkow,Predrag Krajacic,Alyssa Cwanger Weissberger,John T. Connelly,Michael Spino,Michael K. Lee,James R. Connor,Benoit I. Giasson,Z. Leah Harris,Joshua L. Dunaief +20 more
TL;DR: Treatment with the oral iron chelator deferiprone diminished brain iron levels, protected against neuron loss, and extended lifespan in mice with combined mutation of Cp and its homolog hephaestin.
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α-Synucleinopathy associated c-Abl activation causes p53-dependent autophagy impairment
Md. Razaul Karim,Elly E. Liao,Jaekwang Kim,Joyce Meints,Hector Martell Martinez,Olga Pletnikova,Juan C. Troncoso,Michael K. Lee +7 more
TL;DR: The data show that c-Abl activation by α-synucleinopathy causes p53 dependent autophagy deficits and both c- Abl and p53 represent therapeutic target for PD.
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Transgenic models of neurodegenerative diseases
TL;DR: The disease-specific pathology in transgenic mice demonstrates the utility of these models in elucidating pathogenic mechanisms of the disease and in developing therapeutic strategies.
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Antiapoptotic property of human α‐synuclein in neuronal cell lines is associated with the inhibition of caspase‐3 but not caspase‐9 activity
Wenxue Li,Michael K. Lee +1 more
TL;DR: The effects of expressing human α‐Syn variants on the cellular vulnerability to apoptotic stimuli are examined and it is concluded that Huα‐Syn modulates the activity of cleaved caspase‐3 product in neuronal cell lines.