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Yi Lisa Lyu
Researcher at Rutgers University
Publications - 21
Citations - 2088
Yi Lisa Lyu is an academic researcher from Rutgers University. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 10, co-authored 14 publications receiving 1703 citations.
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Journal ArticleDOI
Identification of the molecular basis of doxorubicin-induced cardiotoxicity
Sui Zhang,Xiaobing Liu,Xiaobing Liu,Tasneem Bawa-Khalfe,Long Sheng Lu,Yi Lisa Lyu,Leroy-Fong Liu,Edward T.H. Yeh,Edward T.H. Yeh +8 more
TL;DR: Cardiomyocyte-specific deletion of Top2b (encoding topoisomerase-IIβ) protects cardiomyocytes from doxorubicin-induced DNA double-strand breaks and transcriptome changes that are responsible for defective mitochondrial biogenesis and ROS formation.
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Etoposide Induces ATM-Dependent Mitochondrial Biogenesis through AMPK Activation
TL;DR: It is proposed that ATM-dependent mitochondrial biogenesis may play a role in DNA damage response and ROS regulation, and that defect in ATM- dependence on etoposide could contribute to the manifestations of A-T disease.
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Role of topoisomerase IIβ in the expression of developmentally regulated genes
TL;DR: Results support a role of TopIIβ in activation/repression of developmentally regulated genes at late stages of neuronal differentiation.
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NF-κB Affects Proliferation and Invasiveness of Breast Cancer Cells by Regulating CD44 Expression
TL;DR: Analysis of the role of NF-κB in regulating CD44 expression in triple negative breast cancer cells, MDA-MB-231 and SUM159 provides new insight into the molecular mechanism underlying CD44 regulation but also potential therapeutic targets that may help eliminate chemo- and radiation-resistant cancer cells.
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Genistein induces topoisomerase IIbeta- and proteasome-mediated DNA sequence rearrangements: Implications in infant leukemia.
TL;DR: A model in which genistein-induced Top2beta cleavage complexes are processed by proteasome, leading to the exposure of otherwise Top2 beta-concealed DSBs and subsequent chromosome rearrangements is suggested, and implicate a major role of Top2 Beta and proteasomes in genisteIn-induced infant leukemia.