Q
Qing Sheng Mi
Researcher at Henry Ford Health System
Publications - 10
Citations - 1343
Qing Sheng Mi is an academic researcher from Henry Ford Health System. The author has contributed to research in topics: Kidney & Gene silencing. The author has an hindex of 10, co-authored 10 publications receiving 1109 citations. Previous affiliations of Qing Sheng Mi include Second Military Medical University & Georgia Regents University.
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Journal Article
ATR-Chk2 signaling in p53 activation and DNA damage response during cisplatin-induced apoptosis (Journal of Biological Chemistry (2008) 283, (6572-6583))
TL;DR: It is shown that ATR is specifically activated during cisplatin treatment and co-localizes with H2AX, forming nuclear foci at the site of DNA damage, suggesting an important role for the DNA damage response mediated by ATR-Chk2 in p53 activation and renal cell apoptosis during cisPlatin nephrotoxicity.
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ATR-Chk2 signaling in p53 activation and DNA damage response during cisplatin-induced apoptosis
TL;DR: In this article, the authors demonstrate an early DNA damage response during cisplatin treatment of renal cells and tissues, and demonstrate a critical role for ATR, but not ATM (ataxia telangiectasia mutated) or DNA-PK (DNA-dependent protein kinase), in the activation and apoptosis of kidney cells.
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Targeted Deletion of Dicer from Proximal Tubules Protects against Renal Ischemia-Reperfusion Injury
TL;DR: Evidence for a pathogenic role of Dicer and associated microRNAs in renal IRI is demonstrated by a mouse model in which the proximal tubular cells lack Dicer, a key enzyme for microRNA production.
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microRNAs in kidneys: biogenesis, regulation, and pathophysiological roles.
TL;DR: Although the field of renal miRNA research is still in its infancy and important questions remain, future investigation on miRNA regulation in kidneys has the potential to revolutionize both the diagnosis and treatment of major renal diseases.
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MicroRNA-34a is induced via p53 during cisplatin nephrotoxicity and contributes to cell survival.
TL;DR: The results suggest that miR-34a is induced via p53 during cisplatin nephrotoxicity and may play a cytoprotective role for cell survival and the regulation of microRNAs in renal diseases.