Faculty Research 1990 - 1999

TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells.

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Animal, Apoptosis, Ca(2+)-Calmodulin-Dependent-Protein-Kinase: me, Cell-Line, Chromosome-Mapping, Chromosomes-Human-Pair-13, Cloning-Molecular, Cycloheximide, Enzyme-Activation, Genes-Immediate-Early, Human, Ligands, Membrane-Glycoproteins: ge, me, Membrane-Proteins, Mice, Molecular-Sequence-Data, Organ-Specificity, Polymerase-Chain-Reaction, Receptors-Tumor-Necrosis-Factor: ph, me, Recombinant-Proteins: bi, me, Sequence-Alignment, Sequence-Homology-Amino-Acid, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, T-Lymphocytes, Tacrolimus, Thymus-Gland: me, Translation-Genetic: de

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J Biol Chem 1997 Oct 3;272(40):25190-4




A novel member of the tumor necrosis factor (TNF) cytokine family, designated TRANCE, was cloned during a search for apoptosis-regulatory genes using a somatic cell genetic approach in T cell hybridomas. The TRANCE gene encodes a type II membrane protein of 316 amino acids with a predicted molecular mass of 35 kDa. Its extracellular domain is most closely related to TRAIL, FasL, and TNF. TRANCE is an immediate early gene up-regulated by TCR stimulation and is controlled by calcineurin-regulated transcription factors. TRANCE is most highly expressed in thymus and lymph nodes but not in nonlymphoid tissues and is abundantly expressed in T cells but not in B cells. Cross-hybridization of the mouse cDNA to a human thymus library yielded the human homolog, which encodes a protein 83% identical to the mouse ectodomain. Human TRANCE was mapped to chromosome 13q14 while mouse TRANCE was located to the portion of mouse chromosome 14 syntenic with human chromosome 13q14. A recombinant soluble form of TRANCE composed of the entire ectodomain induced c-Jun N-terminal kinase (JNK) activation in T cells but not in splenic B cells or in bone marrow-derived dendritic cells. These results suggest a role for this TNF-related ligand in the regulation of the T cell-dependent immune response.

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