Requirement of the JIP1 scaffold protein for stress-induced JNK activation

UMMS Affiliation

Howard Hughes Medical Institute and Program in Molecular Medicine; Department of Cancer Biology; Department of Medicine, Division of Diabetes; Department of Pathology

Publication Date


Document Type



*Adaptor Proteins, Signal Transducing; Animals; Apoptosis; Carrier Proteins; Enzyme Activation; JNK Mitogen-Activated Protein Kinases; Mice; Mice, Inbred C57BL; Mice, Knockout; Mitogen-Activated Protein Kinases; Neurons; *Oxidative Stress


Life Sciences | Medicine and Health Sciences


The c-Jun N-terminal kinase (JNK) signal transduction pathway is activated in response to the exposure of cells to environmental stress. Components of the JNK signaling pathway interact with the JIP1 scaffold protein. JIP1 is located in the neurites of primary hippocampal neurons. However, in response to stress, JIP1 accumulates in the soma together with activated JNK and phosphorylated c-Jun. Disruption of the Jip1 gene in mice by homologous recombination prevented JNK activation caused by exposure to excitotoxic stress and anoxic stress in vivo and in vitro. These data show that the JIP1 scaffold protein is a critical component of a MAP-kinase signal transduction pathway.

DOI of Published Version



Genes Dev. 2001 Sep 15;15(18):2421-32. Link to article on publisher's site

Journal/Book/Conference Title

Genes and development

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Link to Article in PubMed

PubMed ID