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Jing Qin

Researcher at Sun Yat-sen University

Publications -  48
Citations -  939

Jing Qin is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Regulation of gene expression & Gene regulatory network. The author has an hindex of 16, co-authored 45 publications receiving 705 citations. Previous affiliations of Jing Qin include The Chinese University of Hong Kong & Li Ka Shing Faculty of Medicine, University of Hong Kong.

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Vitamin D inhibits cox-2 expression and inflammatory response by targeting thioesterase superfamily member 4

TL;DR: It is found that the active form of vitamin D produces dose-dependent inhibition of COX-2 expression in murine macrophages under both basal and LPS-stimulated conditions and suppresses proinflammatory mediators induced by LPS.
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Inferring gene regulatory networks by integrating ChIP-seq/chip and transcriptome data via LASSO-type regularization methods

TL;DR: Two extended models of LASSO, L0 and L1/2 regularization models are applied to infer gene regulatory network from both high-throughput gene expression data and transcription factor binding data in mouse embryonic stem cells to demonstrate the efficiency and applicability of these two models.

ChIP-array: combinatory analysis of ChIP-seq/chip and microarray gene expression data

TL;DR: ChIP-Array is presented, a web server that integrates ChIP-X and expression data from human, mouse, yeast, fruit fly and Arabidopsis to assist biologists to detect direct and indirect target genes regulated by a TF of interest and to aid in the functional characterization of the TF.
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ChIP-Array: combinatory analysis of ChIP-seq/chip and microarray gene expression data to discover direct/indirect targets of a transcription factor

TL;DR: ChIP-Array as discussed by the authors is a web server that integrates ChIP-X and expression data from human, mouse, yeast, fruit fly and Arabidopsis to detect direct and indirect target genes regulated by a transcription factor of interest.
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Inhibition of KAP1 Enhances Hypoxia-Induced Kaposi's Sarcoma-Associated Herpesvirus Reactivation through RBP-Jκ

TL;DR: Inhibition of KAP1 greatly enhanced the association of RBP-Jκ with the HIF-1α complex for driving RTA expression not only in normoxia but also in hypoxia, suggesting that both K AP1 and the concurrence of RBS+HRE within the RTA promoter are essential for KSHV latency andHypoxia-induced lytic reactivation.