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Jian Dong Li

Researcher at Georgia State University

Publications -  101
Citations -  6582

Jian Dong Li is an academic researcher from Georgia State University. The author has contributed to research in topics: Mucin & Signal transduction. The author has an hindex of 43, co-authored 101 publications receiving 6079 citations. Previous affiliations of Jian Dong Li include Osaka University & University of Rochester Medical Center.

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Activation of NF-κB via a Src-dependent Ras-MAPK-pp90rsk pathway is required for Pseudomonas aeruginosa-induced mucin overproduction in epithelial cells

TL;DR: It is shown that P. aeruginosa activates a c-Src-Ras-MEK1/2-MAPK-pp90rsk signaling pathway that leads to activation of nuclear factor NF-kappaB (p65/p50), which binds to a kappaB site in the 5'-flanking region of the M UC2 gene and activates MUC2 mucin transcription and opens up new therapeutic targets for cystic fibrosis.
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Transcriptional activation of mucin by Pseudomonas aeruginosa lipopolysaccharide in the pathogenesis of cystic fibrosis lung disease

TL;DR: It is shown that P. aeruginosa lipopolysaccharide profoundly upregulates transcription of the mucin gene MUC 2 in epithelial cells via inducible enhancer elements and that this effect is blocked by the tyrosine kinase inhibitors genistein and tyr-phostin AG 126.
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Mucin gene (MUC 2 and MUC 5AC) upregulation by Gram-positive and Gram-negative bacteria.

TL;DR: Results from in situ hybridization and RNase protection assays showed that P. aeruginosa upregulates MUC 5AC as well as MUC 2 in both bronchial explants and cultured airway epithelial cells, indicating the existence of a general mechanism by which epithelial Cells respond to the presence of bacteria by increasing mucin synthesis.
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Vitamin D receptor negatively regulates bacterial-stimulated NF-κB activity in intestine

TL;DR: It is demonstrated that commensal and pathogenic bacteria directly regulate colonic epithelial VDR expression and location in vivo and VDR negatively regulates bacterial-induced intestinal NF-kappaB activation and attenuates response to infection.