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Changjiang Xu

Researcher at Rutgers University

Publications -  24
Citations -  5203

Changjiang Xu is an academic researcher from Rutgers University. The author has contributed to research in topics: Gene expression & MAPK/ERK pathway. The author has an hindex of 22, co-authored 23 publications receiving 4857 citations.

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Induction of phase I, II and III drug metabolism/transport by xenobiotics

TL;DR: Drug metabolizing enzymes (DMEs) play central roles in the metabolism, elimination and detoxification of xenobiotics and drugs introduced into the human body, and play crucial roles in response to many polycyclic aromatic hydrocarbon receptors and excretion.
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Activation of Nrf2-antioxidant signaling attenuates NFκB-inflammatory response and elicits apoptosis

TL;DR: In vivo and in vitro data generated from the laboratory suggest that many dietary compounds can differentially regulate Nrf2-mediated antioxidant/anti-inflammatory signaling pathways as the first line defense or induce apoptosis once the cells have been damaged.
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Inhibition of 7,12-dimethylbenz(a)anthracene-induced skin tumorigenesis in C57BL/6 mice by sulforaphane is mediated by nuclear factor E2-related factor 2.

TL;DR: The results show for the first time that Nrf2(-/-) mice are more susceptible to skin tumorigenesis and that the chemopreventive effects of sulforaphane are mediated, at least in part, through NRF2.
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Mechanism of Action of Sulforaphane: Inhibition of p38 Mitogen-Activated Protein Kinase Isoforms Contributing to the Induction of Antioxidant Response Element–Mediated Heme Oxygenase-1 in Human Hepatoma HepG2 Cells

TL;DR: Results indicate that transcriptional activation of Nrf2/ARE is critical in sulforaphane-mediated induction of HO-1, which can be modulated in part by the blockade of p38 MAPK signaling pathway.
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Suppression of NF-kappaB and NF-kappaB-regulated gene expression by sulforaphane and PEITC through IkappaBalpha, IKK pathway in human prostate cancer PC-3 cells.

TL;DR: The inhibition of SFN and PEITC on NF-κB transcriptional activation as well as NF-σκB-regulated VEGF, cyclin D1, and Bcl-XL gene expression is mainly mediated through the inhibition of IKK phosphorylation, particularly IKKβ, and the inhibited of IκBα phosphorylated and degradation, aswell as the decrease of nuclear translocation of p65 in PC-3 cells.