scholarly journals Activation of Phosphatidylinositol 3-Kinase/Akt and Impairment of Nuclear Factor-κB

2010 ◽  
Vol 177 (6) ◽  
pp. 2898-2911 ◽  
Author(s):  
Bruno Miguel Neves ◽  
Ricardo Silvestre ◽  
Mariana Resende ◽  
Ali Ouaissi ◽  
Joana Cunha ◽  
...  
Keyword(s):  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

scholarly journals Interferon α/β Promotes Cell Survival by Activating Nuclear Factor κB through Phosphatidylinositol 3-Kinase and Akt

2001 ◽  
Vol 276 (17) ◽  
pp. 13756-13761 ◽  
Author(s):  
Chuan He Yang ◽  
Aruna Murti ◽  
Susan R. Pfeffer ◽  
Jong G. Kim ◽  
David B. Donner ◽  
...  
Keyword(s):  
Cell Survival ◽  
Nuclear Factor Κb ◽  
Interferon Α ◽  
Nuclear Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

scholarly journals Mechanisms of Glucose-Induced Expression of Pancreatic-Derived Factor in Pancreatic β-Cells

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 672-680 ◽  
Author(s):  
Oumei Wang ◽  
Kun Cai ◽  
Shanshan Pang ◽  
Ting Wang ◽  
Dongfei Qi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Signaling Pathways ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Promoter Activation ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Phosphatidylinositol 3

Pancreatic-derived factor (PANDER) is a cytokine-like peptide highly expressed in pancreatic β-cells. PANDER was reported to promote apoptosis of pancreatic β-cells and secrete in response to glucose. Here we explored the effects of glucose on PANDER expression, and the underlying mechanisms in murine pancreatic β-cell line MIN6 and primary islets. Our results showed that glucose up-regulated PANDER mRNA and protein levels in a time- and dose-dependent manner in MIN6 cells and pancreatic islets. In cells expressing cAMP response element-binding protein (CREB) dominant-negative construct, glucose failed to induce PANDER gene expression and promoter activation. Treatment of the cells with calcium chelator [EGTA, 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid tetra(acetoxymethyl)ester (BAPTA/AM)], the voltage-dependent Ca2+ channel inhibitor (nifedipine), the protein kinase A (PKA) inhibitor (H89), the protein kinase C (PKC) inhibitor (Go6976), or the MAPK kinase 1/2 inhibitor (PD98059), all significantly inhibited glucose-induced PANDER gene expression and promoter activation. Further studies showed that glucose induced CREB phosphorylation through Ca2+-PKA-ERK1/2 and Ca2+-PKC pathways. Thus, the Ca2+-PKA-ERK1/2-CREB and Ca2+-PKC-CREB signaling pathways are involved in glucose-induced PANDER gene expression. Wortmannin (phosphatidylinositol 3-kinase inhibitor), ammonium pyrrolidinedithiocarbamate (nuclear factor-κB inhibitor and nonspecific antioxidant), and N-acetylcysteine (antioxidant) were also found to inhibit glucose-induced PANDER promoter activation and gene expression. Because there is no nuclear factor-κB binding site in the promoter region of PANDER gene, these results suggest that phosphatidylinositol 3-kinase and reactive oxygen species be involved in glucose-induced PANDER gene expression. In conclusion, glucose induces PANDER gene expression in pancreatic β-cells through multiple signaling pathways. Because PANDER is expressed by pancreatic β-cells and in response to glucose in a similar way to those of insulin, PANDER may be involved in glucose homeostasis.

scholarly journals Resveratrol Modulates Interleukin-1β-induced Phosphatidylinositol 3-Kinase and Nuclear Factor κB Signaling Pathways in Human Tenocytes

2012 ◽  
Vol 287 (45) ◽  
pp. 38050-38063 ◽  
Author(s):  
Franziska Busch ◽  
Ali Mobasheri ◽  
Parviz Shayan ◽  
Cora Lueders ◽  
Ralf Stahlmann ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Nuclear Factor Κb ◽  
Interleukin 1Β ◽  
Nuclear Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3
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