SF1126, a Novel Integrin-Targeting Phosphatidylinositol-3 Kinase Inhibitor, Has Radiosensitizing and Anti-Tumor Effects in Glioma Model Systems

2007 ◽  
Vol 69 (3) ◽  
pp. S98
Author(s):  
H.G. Shu ◽  
H. Gao ◽  
C. Chang ◽  
D.L. Durden
Keyword(s):  
Kinase Inhibitor ◽  
Model Systems ◽  
Phosphatidylinositol 3 Kinase ◽  
Glioma Model ◽  
Phosphatidylinositol 3

scholarly journals In Vitro Antimetastatic Effect of Phosphatidylinositol 3-Kinase Inhibitor ZSTK474 on Prostate Cancer PC3 Cells

2013 ◽  
Vol 14 (7) ◽  
pp. 13577-13591 ◽  
Author(s):  
Wennan Zhao ◽  
Wenzhi Guo ◽  
Qianxiang Zhou ◽  
Sheng-Nan Ma ◽  
Ran Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Kinase Inhibitor ◽  
Phosphatidylinositol 3 Kinase ◽  
Antimetastatic Effect ◽  
Pc3 Cells ◽  
Phosphatidylinositol 3

scholarly journals Aquaporins and Fetal Membranes From Diabetic Parturient Women: Expression Abnormalities and Regulation by Insulin

2015 ◽  
Vol 100 (10) ◽  
pp. E1270-E1279 ◽  
Author(s):  
Damien Bouvier ◽  
Marion Rouzaire ◽  
Geoffroy Marceau ◽  
Cécile Prat ◽  
Bruno Pereira ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Kinase Inhibitor ◽  
Fetal Membranes ◽  
Phosphatidylinositol 3 Kinase ◽  
Intracellular Signaling Pathway ◽  
The Impact ◽  
Phosphatidylinositol 3

Context: During pregnancy, aquaporins (AQPs) expressed in fetal membranes are essential for controlling the homeostasis of the amniotic volume, but their regulation by insulin was never explored in diabetic women. Objective: The aim of our study was to investigate the involvement of AQPs 1, 3, 8, and 9 expressed in fetal membranes in diabetic parturient women and the control of their expression by insulin. Design and Participants: From 129 fetal membranes in four populations (controls, type 1, type 2 [T2D], and gestational diabetes [GD]), we established an expression AQP profile. In a second step, the amnion was used to study the control of the expression and functions of AQPs 3 and 9 by insulin. Main Outcomes and Measures: The expression of transcripts and proteins of AQPs was studied by quantitative RT-PCR and ELISA. We analyzed the regulation by insulin of the expression of AQPs 3 and 9 in the amnion. A tritiated glycerol test enabled us to measure the impact of insulin on the functional characteristics. Using an inhibitor of phosphatidylinositol 3-kinase, we analyzed the insulin intracellular signaling pathway. Results: The expression of AQP3 protein was significantly weaker in groups T2D and GD. In nondiabetic fetal membranes, we showed for the amnion (but not for the chorion) a significant repression by insulin of the transcriptional expression of AQPs 3 and 9, which was blocked by a phosphatidylinositol 3-kinase inhibitor. Conclusion: In fetal membranes, the repression of AQP3 protein expression and functions observed in vivo is allowed by the hyperinsulinism described in pregnant women with T2D or GD.

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