Physiological Concentrations of Insulin Augment Pancreatic Cancer Cell Proliferation and Glucose Utilization By Activating MAP Kinase, PI_3 Kinase and Enhancing GLUT-1 Expression
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概要
- 論文の詳細を見る
- 2000-10-01
著者
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Adrian Thomas
Department Of Biomedical Sciences Creighton University School Of Medicine
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Murphy Leon
Department Of Biomedical Sciences Creighton University School Of Medicine
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Adrian Thomas
Department Of Biomedical Sciences And Cancer Center Creighton University School Of Medicine
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PERMERT Johan
Department of Surgery, Karolinska Institute, Huddinge Hospital
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DING Xian-Zhong
Department of Biomedical Sciences, Creighton University School of Medicine
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FEHSENFELD Drew
Department of Biomedical Sciences, Creighton University School of Medicine
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Fehsenfeld Drew
Department Of Biomedical Sciences Creighton University School Of Medicine
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Ding Xian-zhong
Department Of Biomedical Sciences Creighton University School Of Medicine
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Permert Johan
Department Of Surgery Karolinska Institute Huddinge Hospital
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Permert Johan
Department Of Surgery Karolinska Institute At Huddinge University Hospital
関連論文
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- Physiological Concentrations of Insulin Augment Pancreatic Cancer Cell Proliferation and Glucose Utilization By Activating MAP Kinase, PI_3 Kinase and Enhancing GLUT-1 Expression
- On the Importance of Cholecystokinin in Neonatal Pancreatic Growth and Secretory Development in Guinea Pigs
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- The Role of Oxygen-Derived Free Radicals and Nitric Oxide in Cytokine-Induced Antiproliferation of Pancreatic Cancer Cells
- Dissociated Insulin and Islet Amyloid Polypeptide Secretion from Isolated Rat Pancreatic Islets Cocultured with Human Pancreatic Adenocarcinoma Cells
- Differential Inhibition of Insulin and Islet Amyloid Polypeptide Secretion by Intraislet Somatostatin in the Isolated Perfused Human Pancreas
- The Regulation of Amylin and Insulin Gene Expression and Secretion
- Arsenic Trioxide Induces Apoptosis in Pancreatic Cancer Cells via Changes in Cell Cycle, Caspase Activation, and GADD Expression
- The Intracellular Mechanism of Insulin Resistance in the Hamster Pancreatic Ductal Adenocarcinoma Model