Requirement of the JIP1 scaffold protein for stress-induced JNK activation
AuthorsWhitmarsh, Alan J.
Kennedy, Norman J.
Haydar, Tarik F.
Mordes, John P.
Appel, Michael C.
Rossini, Aldo A.
Jones, Stephen N.
Flavell, Richard A.
Davis, Roger J.
UMass Chan AffiliationsDepartment of Pathology
Department of Medicine, Division of Diabetes
Department of Cancer Biology
Howard Hughes Medical Institute and Program in Molecular Medicine
Keywords*Adaptor Proteins, Signal Transducing
JNK Mitogen-Activated Protein Kinases
Mice, Inbred C57BL
Mitogen-Activated Protein Kinases
Medicine and Health Sciences
MetadataShow full item record
AbstractThe 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.
Genes Dev. 2001 Sep 15;15(18):2421-32. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/42222
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