Kelkar, NyayaGupta, ShashiDickens, MartinDavis, Roger J.2022-08-232022-08-232000-01-112009-03-24Mol Cell Biol. 2000 Feb;20(3):1030-43.0270-7306 (Print)10629060https://hdl.handle.net/20.500.14038/38572The 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.en-US*Adaptor Proteins, Signal TransducingAgingAmino Acid SequenceAnimalsBrainCells, CulturedCloning, MolecularEmbryonic and Fetal DevelopmentEnzyme ActivationFemale*Gene Expression Regulation, DevelopmentalGene LibraryJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase KinasesMaleMiceMitogen-Activated Protein KinasesMolecular Sequence DataNerve Tissue ProteinsNeuronsProtein IsoformsRecombinant ProteinsSequence AlignmentSequence Homology, Amino AcidSignal TransductionLife SciencesMedicine and Health SciencesJournal Articlehttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2438&context=oapubs&unstamped=1https://escholarship.umassmed.edu/oapubs/1439794936oapubs/1439