Xiaoqi Liu
Purdue University
111 Papers
382 Citations
Xiaoqi Liu is an academic researcher from Purdue University. The author has contributed to research in topics: PLK1 & Prostate cancer. The author has an hindex of 39, co-authored 99 publications. Previous affiliations of Xiaoqi Liu include Harvard University & Washington State University.
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Papers
Chemical visualization of phosphoproteomes on membrane
TL;DR: The chemical reagent, which is termed pIMAGO, is based on a multifunctionalized soluble nanopolymer and is capable of selectively binding to phosphorylated residues independent of amino acid microenvironment, thus offering great promise as a universal tool in biological analyses where the site of phosphorylation is not known or its specific antibody is not available.
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Ultraviolet damage and nucleosome folding of the 5S ribosomal RNA gene.
TL;DR: Modulation of the CPD distribution in a 14 nt long pyrimidine tract correlates with its rotational setting on the histone surface, when the strong sequence bias for CPD formation in this tract is minimized by normalization, to establish the mutual roles of histone binding and UV photoproducts on their formation in chromatin.
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Cdc2-mediated Phosphorylation of CLIP-170 Is Essential for Its Inhibition of Centrosome Reduplication
TL;DR: It is found that depletion of CLIP-170 leads to centrosome reduplication and that Cdc2 phosphorylation of CLip-170 is required for the process, demonstrating that CDC2-mediated phosphorylates this protein is essential for the normal function of this protein during cell cycle progression.
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Polo-like kinase 1 (Plk1) overexpression enhances ionizing radiation-induced cancer formation in mice
Zhiguo Li,Jinghui Liu,Jie Li,Yifan Kong,George E. Sandusky,Xi Rao,Yunlong Liu,Jun Wan,Xiaoqi Liu +8 more
TL;DR: In this paper, the role of Plk1 in tumorigenesis was investigated using a conditional expression system, and it was shown that Plk 1 overexpression may contribute to tumor formation by both inducing chromosomal instability and suppressing the DDR pathway.
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Combining p53 stabilizers with metformin induces synergistic apoptosis through regulation of energy metabolism in castration-resistant prostate cancer
Long Chen,Nihal Ahmad,Xiaoqi Liu +2 more
TL;DR: Of significance, castration-resistant prostate cancer (CRPC) C4-2 cells show a much more robust response to the combination treatment than the parental androgen-dependent prostate cancer LNCaP cells, indicating that targeting energy metabolism with metformin plus p53 stabilizers might be a valid approach to treat CRPC carrying WT p53.
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