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  • 1995-1999  (3)
  • 1
    Electronic Resource
    Electronic Resource
    GENOMIC IMPRINTING IN MAMMALS (1997)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Genetics 31 (1997), S. 493-525 
    Details
    ISSN: 0066-4197
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology
    Notes: Abstract A handful of autosomal genes in the mammalian genome are inherited in a silent state from one of the two parents, and in a fully active form from the other, thereby rendering the organism functionally hemizygous for imprinted genes. To date 19 imprinted genes have been identified; 5 are expressed from the maternal chromosome while the rest are expressed from the paternal chromosome. Allele-specific methylation of CpG residues, established in one of the germlines and maintained throughout embryogenesis, has been clearly implicated in the maintenance of imprinting in somatic cells. Although the function of imprinting remains a subject of some debate, the process is thought to have an important role in regulating the rate of fetal growth.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.genet.31.1.493
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    A paternal–specific methylation imprint marks the alleles of the mouse H19 gene (1995)
    [s.l.] : Nature Publishing Group
    Nature genetics 9 (1995), S. 407-413 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Imprinting, the differential expression of the two alleles of a gene based on their parental origin, requires that the alleles be distinguished or marked. A candidate for the differentiating mark is DNA methylation. The maternally expressed H19 gene is hypermethylated on the inactive paternal ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng0495-407
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Clustered α-amanitin resistance mutations in mouse (1995)
    Springer
    Molecular genetics and genomics 246 (1995), S. 778-782 
    Details
    ISSN: 1617-4623
    Keywords: RNA polymerase II ; α-Amanitin Mutation ; Transcription
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract We report the identification of three new α-amanitin resistance mutations in the gene encoding the largest subunit of mouse RNA polymerase II (RPII215). These mutations are clustered in a region of the largest subunit that is important for transcription elongation. This same domain has been identified as the site of α-amanitin resistance mutations in both Drosophila and Caenarhabditis elegans. The sequences encompassing this cluster of mutations are highly conserved among RNA polymerase II genes from a number of species, including those that are naturally more resistant to α-amanitin suggesting that this region of the largest subunit is critical for a conserved catalytic function. The mutations reported here change leucine 745 to phenylalanine, arginine 749 to proline, or isoleucine 779 to phenylalanine. Together with the previously reported asparagine 792 to aspartate substitution these mutations define a potential α-amanitin binding pocket in a region of the mouse subunit that could be involved in translocation of polymerase during elongation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00290727
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    Paper (German National Licenses)
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