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  • 1
    Electronic Resource
    Electronic Resource
    Genomic Organization and Regulation of the Human Interleukin-18 Gene (2000)
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 52 (2000), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The human interleukin(IL)-18 is a key regulator of interferon(IFN)-γ production and T-cell differentiation. Here we report the complete genomic structure and characterization of the 5′untranslated promoter region of the human IL-18 gene. The gene is composed of six exons and five introns, spanning approximately 19.5kb. Promoter activity of the 5′-flanking region was investigated with a luciferase reporter gene assay. Transient transfection studies demonstrate a constitutive expression of the IL-18 gene in monocytic U937 and THP-1 cells. For this constitutive expression at least 92 base pairs of the promoter region are essential as shown by consecutive 5′ promoter deletions in both cell types. DNA protein binding experiments revealed specific binding of activated signal transducer and activator of transcription factor-5 (STAT5) but not of STAT3 to three consensus sequences upstream in the promoter region. Cotransfection of STAT5 resulted in increased induction of the IL-18 promoter in the U937 and THP-1 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.2000.00836.x
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  • 2
    Electronic Resource
    Electronic Resource
    Incidence of ras gene mutations in neuroblastoma (1988)
    Springer
    European journal of pediatrics 147 (1988), S. 313-314 
    Details
    ISSN: 1432-1076
    Keywords: Neuroblastoma ; Oncogene ; ras gene ; Molecular genetics ; Polymerase chain reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Using a rapid dot-blot screening procedure based on DNA amplification and hybridization to synthetic oligonucleotide probes, we investigated 18 neuroblastomas in various clinical stages for the presence of ras mutations. In none of the samples was a mutation in the relevant codons 12, 13 or 61 of Ha-ras, Ki-ras or N-ras found. These data virtually exclude the participation of mutated ras genes in the genesis of neuroblastoma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00442704
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    Paper (German National Licenses)
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