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Akt1 regulates a JNK scaffold during excitotoxic apoptosis.

Neuron | Aug 15, 2002

Cell survival is determined by a balance among signaling cascades, including those that recruit the Akt and JNK pathways. Here we describe a novel interaction between Akt1 and JNK interacting protein 1 (JIP1), a JNK pathway scaffold. Direct association between Akt1 and JIP1 was observed in primary neurons. Neuronal exposure to an excitotoxic stimulus decreased the Akt1-JIP1 interaction and concomitantly increased association between JIP1 and JNK. Akt1 interaction with JIP1 inhibited JIP1-mediated potentiation of JNK activity by decreasing JIP1 binding to specific JNK pathway kinases. Consistent with this view, neurons from Akt1-deficient mice exhibited higher susceptibility to kainate than wild-type littermates. Overexpression of Akt1 mutants that bind JIP1 reduced excitotoxic apoptosis. These results suggest that Akt1 binding to JIP1 acts as a regulatory gate preventing JNK activation, which is released under conditions of excitotoxic injury.

Pubmed ID: 12194869 RIS Download

Mesh terms: Adaptor Proteins, Signal Transducing | Animals | Apoptosis | Arabidopsis Proteins | Carrier Proteins | Cell Survival | Cells, Cultured | Central Nervous System Diseases | Fetus | Gene Deletion | Gene Expression | Glutamic Acid | Hippocampus | Humans | JNK Mitogen-Activated Protein Kinases | Kainic Acid | Mice | Mice, Knockout | Mitogen-Activated Protein Kinases | Neurons | Neurotoxins | Plant Proteins | Potassium Channels | Protein Binding | Rats | Rats, Sprague-Dawley | Receptors, Glutamate | Signal Transduction

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Associated grants

  • Agency: NCI NIH HHS, Id: CA56490
  • Agency: NICHD NIH HHS, Id: HD23315
  • Agency: NINDS NIH HHS, Id: NS21072

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