UMMS Affiliation

Howard Hughes Medical Institute, Program in Molecular Medicine

Date

1-11-2000

Document Type

Article

Subjects

*Adaptor Proteins, Signal Transducing; Aging; Amino Acid Sequence; Animals; Brain; Cells, Cultured; Cloning, Molecular; Embryonic and Fetal Development; Enzyme Activation; Female; *Gene Expression Regulation, Developmental; Gene Library; JNK Mitogen-Activated Protein Kinases; MAP Kinase Kinase Kinases; Male; Mice; Mitogen-Activated Protein Kinases; Molecular Sequence Data; Nerve Tissue Proteins; Neurons; Protein Isoforms; Recombinant Proteins; Sequence Alignment; Sequence Homology, Amino Acid; Signal Transduction

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

The c-Jun NH(2)-terminal kinase (JNK) group of mitogen-activated protein kinases (MAPKs) is activated in response to the treatment of cells with inflammatory cytokines and by exposure to environmental stress. JNK activation is mediated by a protein kinase cascade composed of a MAPK kinase and a MAPK kinase kinase. Here we describe the molecular cloning of a putative molecular scaffold protein, JIP3, that binds the protein kinase components of a JNK signaling module and facilitates JNK activation in cultured cells. JIP3 is expressed in the brain and at lower levels in the heart and other tissues. Immunofluorescence analysis demonstrated that JIP3 was present in the cytoplasm and accumulated in the growth cones of developing neurites. JIP3 is a member of a novel class of putative MAPK scaffold proteins that may regulate signal transduction by the JNK pathway.

Rights and Permissions

Citation: Mol Cell Biol. 2000 Feb;20(3):1030-43.

Related Resources

Link to Article in PubMed

Journal Title

Molecular and cellular biology

PubMed ID

10629060

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