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Qiang Liu

Researcher at Chinese Academy of Sciences

Publications -  209
Citations -  9439

Qiang Liu is an academic researcher from Chinese Academy of Sciences. The author has contributed to research in topics: Catalysis & LRP1. The author has an hindex of 50, co-authored 190 publications receiving 7593 citations. Previous affiliations of Qiang Liu include Xiamen University & Laboratory of Molecular Biology.

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Benzoxazole-Linked Ultrastable Covalent Organic Frameworks for Photocatalysis.

TL;DR: This contribution represents the first report on the photocatalytic application of benzoxazole-based structures and sheds new light on the exploration of robust organophotocatalysts from small molecules to extended frameworks but also offers in-depth understanding of the structure-activity relationship toward practical applications of COF materials.
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3D Flowerlike Ceria Micro/Nanocomposite Structure and Its Application for Water Treatment and CO Removal

TL;DR: In this paper, a simple and economical route based on ethylene glycol mediated process was developed to synthesize three-dimensional (3D) flowerlike ceria micro/nanocomposite structure using cerium chloride as a reactant.
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Cholesterol metabolism and homeostasis in the brain.

TL;DR: This review will seek to integrate current knowledge about the brain cholesterol metabolism with molecular mechanisms and show how cholesterol metabolism and its complex homeostasis regulation are currently poorly understood.
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U1 snRNP Determines mRNA Length and Regulates Isoform Expression

TL;DR: It is shown that rapid and transient transcriptional upregulation inherent to neuronal activation physiology creates U1 shortage relative to pre-mRNAs, and additional experiments suggest cotranscriptional PCPA counteracted by U1 association with nascent transcripts, a process the authors term telescripting, ensuring transcriptome integrity and regulating mRNA length.
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Amyloid Precursor Protein Regulates Brain Apolipoprotein E and Cholesterol Metabolism through Lipoprotein Receptor LRP1

TL;DR: It is found that deletion of APP and its homolog APLP2, or components of the gamma-secretase complex, significantly enhanced the expression and function of LRP1, which was reversed by forced expression of the APP intracellular domain (AICD).