ERK activation is required for CCK-mediated pancreatic adaptive growth in mice

High levels of cholecystokinin (CCK) can stimulate pancreatic adaptive growth in which mature acinar cells divide, leading to enhanced pancreatic mass with parallel increases in protein, DNA, RNA, and digestive enzyme content. Prolonged release of CCK can be induced by feeding trypsin inhibitor (TI)...

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Veröffentlicht in:	American journal of physiology: Gastrointestinal and liver physiology 2014-10, Vol.307 (7), p.G700-G710
Hauptverfasser:	Holtz, Bryan J, Lodewyk, Kevin B, Sebolt-Leopold, Judith S, Ernst, Stephen A, Williams, John A
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cell cycle Cell Cycle Proteins - metabolism Cell Proliferation - drug effects Cholecystokinin - metabolism Deoxyribonucleic acid DNA DNA Replication Early Growth Response Transcription Factors - metabolism Enzyme Activation Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors Extracellular Signal-Regulated MAP Kinases - metabolism Genes Male MAP Kinase Signaling System - drug effects Mice, Inbred ICR Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinase Kinases - metabolism Pancreas Pancreas - drug effects Pancreas - enzymology Pancreas - growth & development Protein Kinase Inhibitors - pharmacology Proteins RNA - biosynthesis Rodents Time Factors Trypsin Inhibitors - pharmacology
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