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Träfflista för sökning "(L773:1546 1718) srt2:(2000-2004) srt2:(2000)"

Search: (L773:1546 1718) srt2:(2000-2004) > (2000)

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  • Horikawa, Y, et al. (author)
  • Genetic variation in the gene encoding calpain-10 is associated with type 2 diabetes mellitus
  • 2000
  • In: Nature Genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 26:2, s. 163-175
  • Journal article (peer-reviewed)abstract
    • Type 2 or non-insulin-dependent diabetes mellitus (NIDDM) is the most common form of diabetes worldwide, affecting approximately 4% of the world's adult population. It is multifactorial in origin with both genetic and environmental factors contributing to its development. A genome-wide screen for type 2 diabetes genes carried out in Mexican Americans localized a susceptibility gene, designated NIDDM1, to chromosome 2. Here we describe the positional cloning of a gene located in the NIDDM1 region that shows association with type 2 diabetes in Mexican Americans and a Northern European population from the Botnia region of Finland. This putative diabetes-susceptibility gene encodes a ubiquitously expressed member of the calpain-like cysteine protease family, calpain-10 (CAPN10). This finding suggests a novel pathway that may contribute to the development of type 2 diabetes.
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3.
  • Jimenez, Gretchen S., et al. (author)
  • A transactivation-deficient mouse model provides insights into trp53 regulation and function
  • 2000
  • In: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 26:1, s. 37-43
  • Journal article (peer-reviewed)abstract
    • The gene Trp53 is among the most frequently mutated and studied genes in human cancer, but the mechanisms by which it suppresses tumour formation remain unclear. We generated mice with an allele encoding changes at Leu25 and Trp26, known to be essential for transcriptional transactivation and Mdm2 binding, to enable analyses of Trp53 structure and function in vivo. The mutant Trp53 was abundant, its level was not affected by DNA damage and it bound DNA constitutively; however, it showed defects in cell-cycle regulation and apoptosis. Both mutant and Trp53-null mouse embryonic fibroblasts (MEFs) were readily transformed by oncogenes, and the corresponding mice were prone to tumours. We conclude that the determining pathway for Trp53 tumour-suppressor function in mice requires the transactivation domain.
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4.
  • Krings, M, et al. (author)
  • A view of Neandertal genetic diversity
  • 2000
  • In: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 26:2, s. 144-146
  • Journal article (peer-reviewed)
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