1. Cloning of a gene (RIG-G) associated with retinoic acid-induced differentiation of acute promyelocytic leukemia cells and representing a new member of a family of interferon-stimulated genes.
- Author
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Yu M, Tong JH, Mao M, Kan LX, Liu MM, Sun YW, Fu G, Jing YK, Yu L, Lepaslier D, Lanotte M, Wang ZY, Chen Z, Waxman S, Wang YX, Tan JZ, and Chen SJ
- Subjects
- Amino Acid Sequence, Base Sequence, Cell Differentiation drug effects, Cell Differentiation genetics, Chromosome Mapping, Cloning, Molecular, Genes, Tumor Suppressor, Humans, Intracellular Signaling Peptides and Proteins, Leukemia, Promyelocytic, Acute pathology, Molecular Sequence Data, Sequence Alignment, Tumor Cells, Cultured, Antineoplastic Agents pharmacology, Chromosomes, Human, Pair 10, Interferons genetics, Leukemia, Promyelocytic, Acute genetics, Proteins genetics, Tretinoin pharmacology
- Abstract
In a cell line (NB4) derived from a patient with acute promyelocytic leukemia, all-trans-retinoic acid (ATRA) and interferon (IFN) induce the expression of a novel gene we call RIG-G (for retinoic acid-induced gene G). This gene codes for a 58-kDa protein containing 490 amino acids with several potential sites for post-translational modification. In untreated NB4 cells, the expression of RIG-G is undetectable. ATRA treatment induces the transcriptional expression of RIG-G relatively late (12-24 hr) in a protein synthesis-dependent manner, whereas IFN-alpha induces its expression early (30 min to 3 hr). Database search has revealed a high-level homology between RIG-G and several IFN-stimulated genes in human (ISG54K, ISG56K, and IFN-inducible and retinoic acid-inducible 58K gene) and some other species, defining a well conserved gene family. The gene is composed of two exons and has been mapped by fluorescence in situ hybridization to chromosome 10q24, where two other human IFN-stimulated gene members are localized. A synergistic induction of RIG-G expression in NB4 cells by combined treatment with ATRA and IFNs suggests that a collaboration exists between their respective signaling pathways.
- Published
- 1997
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