Title : TLR3-mediated NF-{kappa}B signaling in human esophageal epithelial cells.

Pub. Date : 2009 Dec

PMID : 19779021






4 Functional Relationships(s)
Download
Sentence
Compound Name
Protein Name
Organism
1 Through reporter gene studies, we show that poly(I:C)-induced NF-kappaB activation is critical for the transactivation of the IL-8 promoter in vitro and that nuclear translocation of NF-kappaB occurs at an early time point following poly(I:C) stimulation of esophageal epithelial cells. Poly I-C nuclear factor kappa B subunit 1 Homo sapiens
2 Through reporter gene studies, we show that poly(I:C)-induced NF-kappaB activation is critical for the transactivation of the IL-8 promoter in vitro and that nuclear translocation of NF-kappaB occurs at an early time point following poly(I:C) stimulation of esophageal epithelial cells. Poly I-C nuclear factor kappa B subunit 1 Homo sapiens
3 Importantly, we also show that poly(I:C) stimulation induces the NF-kappaB-dependent esophageal epithelial expression of TLR2, leading to enhanced epithelial responsiveness of EPC2-hTERT cells to TLR2 ligand stimulation, suggesting an important regulatory role for TLR3-mediated NF-kappaB signaling in the innate immune response of esophageal epithelial cells. Poly I-C nuclear factor kappa B subunit 1 Homo sapiens
4 Importantly, we also show that poly(I:C) stimulation induces the NF-kappaB-dependent esophageal epithelial expression of TLR2, leading to enhanced epithelial responsiveness of EPC2-hTERT cells to TLR2 ligand stimulation, suggesting an important regulatory role for TLR3-mediated NF-kappaB signaling in the innate immune response of esophageal epithelial cells. Poly I-C nuclear factor kappa B subunit 1 Homo sapiens