Abstract
Jun N-terminal kinase (JNK) regulates the transcription factor AP-1, which is implicated in the controlled expression of many genes involved in the immune response. For this reason, drug discovery efforts have focused on the development of JNK inhibitors for chronic inflammatory diseases. However, recent genetic evidence and emerging pharmacological data indicate that activated JNK could be critical in causing diabetes, insulin resistance and obesity. Indeed, if JNK is considered as a stress-activated protein kinase, there appear to be multiple mechanisms through which it might promote diabetes.
MeSH terms
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Animals
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Diabetes Mellitus, Type 2 / drug therapy*
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Diabetes Mellitus, Type 2 / immunology
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Diabetes Mellitus, Type 2 / metabolism
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Drug Delivery Systems
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Enzyme Activation
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Humans
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Insulin Resistance
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JNK Mitogen-Activated Protein Kinases*
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MAP Kinase Kinase 4
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Mice
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Mitogen-Activated Protein Kinase Kinases / genetics
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Mitogen-Activated Protein Kinase Kinases / metabolism
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Mitogen-Activated Protein Kinase Kinases / physiology*
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Pancreas / immunology
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Pancreas / metabolism
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Receptor, Insulin / physiology
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Signal Transduction
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Tumor Necrosis Factor-alpha / physiology
Substances
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Tumor Necrosis Factor-alpha
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Receptor, Insulin
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JNK Mitogen-Activated Protein Kinases
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MAP Kinase Kinase 4
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Mitogen-Activated Protein Kinase Kinases