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Xiaoli Qu

Researcher at Zhengzhou University

Publications -  17
Citations -  415

Xiaoli Qu is an academic researcher from Zhengzhou University. The author has contributed to research in topics: Erythropoiesis & Biology. The author has an hindex of 5, co-authored 11 publications receiving 125 citations. Previous affiliations of Xiaoli Qu include New York Blood Center & Henan Agricultural University.

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Carbon dots as a new class of nanomedicines: Opportunities and challenges

TL;DR: This review provides concise insights into the recent development of CDs in nanomedicine research, including preparation and functionalization processes, and a few critical applications are highlighted, such as antibacterial applications, chemotherapy, and therapeutics.
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Carbon Dots in Bioimaging, Biosensing and Therapeutics: A Comprehensive Review

TL;DR: Carbon dots (CDs) are currently attracting a lot of interest in biological fields owing to their fluorescent properties, high photostability, biocompatibility and low toxicity as discussed by the authors .
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Distinct roles for TET family proteins in regulating human erythropoiesis

TL;DR: It is shown here that TET2 and TET3 but not TET1 are expressed in human erythroid cells, and the role of these proteins in erythropoiesis is explored, to provide new insights into their role in regulating human ERYthroid differentiation at distinct stages of development.
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TET2 deficiency leads to stem cell factor-dependent clonal expansion of dysfunctional erythroid progenitors

TL;DR: It is shown that TET2 deficiency leads initially to stem cell factor-dependent hyperproliferation and impaired differentiation of human colony-forming unit-erythroid (CFU-E) cells, which were reversed by a c-Kit inhibitor, and previously unknown mechanisms by which deficiency of TET1 contributes to ineffective erythropoiesis are uncovered.
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Hypermethylation of Sp1 Binding Site Suppresses Hypothalamic POMC in Neonates and May Contribute to Metabolic Disorders in Adults: Impact of Maternal Dietary CLAs

TL;DR: In cultured cells, the methylation of the −100 CpG dinucleotides of the POMC promoter blocked both the formation of Sp1–promoter complex and the leptin-induced activation of PomC, suggesting that this CLA-mediated hypermethylation may contribute, at least in part, to the metabolic disorders.