Mechanism of interferon-gamma induced increase in intestinal epithelial tight junction permeability: Role of JNK pathway and cross-talk with the PI-3 kinase pathway

被引：0

作者：

Roy, Praveen K.

Chen, Jing

Rashid, Farzana

Ridenhour, Suzanne

Ibdah, Jamal A.

机构：

来源：

GASTROENTEROLOGY | 2008年 / 134卷 / 04期

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暂无

中图分类号：

R57 [消化系及腹部疾病];

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摘要：

引用

页码：A36 / A36

页数：1

共 41 条

[31] Interferon-gamma (IFN γ) induced epithelial barrier dysfunction in T84 human intestinal epithelial cells (IECs) occurs via phosphatidylinositol 3-kinase (PI3-K) mediated activation of adenosine monophosphate-activated protein kinase (AMPK)
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[32] B cell receptor (BCR) cross-talk: IL-4 creates an alternate pathway for BCR-induced ERK activation that is phosphatidylinositol 3-kinase independent
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[33] Comparison of the effects of insulin, PDGF, interleukin-6, and interferon-gamma on glucose transport in 3T3-L1 cells: Lack of cross-talk between tyrosine kinase receptors and JAK/STAT pathways
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[34] Active PI-3 kinase/Akt2 signaling pathway is found in lipid rafts of the Caco-2 colon cancer cell line but not normal intestinal epithelial cells: Possible implications for tumorigenesis
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[36] G protein-coupled receptors (GPCRs) That Signal via Protein Kinase A (PKA) Cross-talk at Insulin Receptor Substrate 1 (IRS1) to Activate the phosphatidylinositol 3-kinase (PI3K)/AKT Pathway
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[37] Role of PI-3-kinase in the mechanism of oxidative stress-induced disruption of tight junction in Caco-2 cell monolayer: Activation of c-Src and FAK
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[38] Bifidobacterium bifidum prevents the IL-1B induced increase in intestinal permeability by a novel mechanism: TLR-2 dependent activation of PPAR-gamma and inhibition of NF-kB signaling pathway
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[39] Increased Sp1 phosphorylation as a mechanism of hepatocyte growth factor (HGF/SF)-induced transcription of vascular endothelial growth factor (VEGF/VPF): contribution of the PI-3 kinase/Akt and MEK1/2 signaling pathway
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[40] B cell receptor (BCR) cross-talk:: CD40 engagement creates an alternate pathway for BCR signaling that activates IκB kinase/IκBα/NF-κB without the need for PI3K and phospholipase Cγ
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