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  • Journal article
    Abramson J, Larsson G, Byrne B, Puustinen A, Garcia-Horsman A, Iwata Set al., 2000,

    Purification, crystallization and preliminary crystallographic studies of an integral membrane protein, cytochrome <i>bo</i><sub>3</sub> ubiquinol oxidase from <i>Escherichia coli</i>

    , ACTA CRYSTALLOGRAPHICA SECTION D-STRUCTURAL BIOLOGY, Vol: 56, Pages: 1076-1078, ISSN: 2059-7983
    • Cite
    • Citations: 11
  • Journal article
    Abecasis GR, Cookson WO, Cardon LR, 2000,

    Pedigree tests of transmission disequilibrium.

    , Eur J Hum Genet, Vol: 8, Pages: 545-551, ISSN: 1018-4813

    High-resolution mapping is essential for the positional cloning of complex disease genes. In outbred populations, linkage disequilibrium is expected to extend for short distances and could provide a powerful fine-mapping tool. Current family-based association tests use nuclear family members to define allelic transmission and controls, but ignore other types of relatives. Here we construct a general approach for scoring allelic transmission that accommodates families of any size and uses all available genotypic information. Family data allows for the construction of an expected genotype for every non-founder, and orthogonal deviates from this expectation are a measure of allelic transmission. These allelic transmission scores can be used to extend previously described tests of linkage disequilibrium for dichotomous or quantitative traits. Some of these tests are illustrated, together with a permutation framework for estimating exact significance levels. Simulation studies are used to investigate power and error rates of the approach. As a practical application, the method is used to investigate the relationship between circulating angiotensin-1 converting enzyme (ACE) levels and polymorphisms in the ACE gene using previously published data.
  • Journal article
    Adcock IM, Ito K, 2000,

    Molecular mechanisms of corticosteroid actions.

    , Monaldi Arch Chest Dis, Vol: 55, Pages: 256-266, ISSN: 1122-0643

    Corticosteroids are the most effective therapy for the treatment of inflammatory diseases such as asthma. Functionally, they act partly by inducing anti-inflammatory genes such as secretary leukocyte proteinase inhibitor, Lipocortin-1 and interleukin-1 receptor antagonist, but mainly by repression of inflammatory genes, such as cytokines, adhesion molecules, inflammatory enzymes and receptors. They act by binding to a cytosolic glucocorticoid receptor (GR), which upon binding is activated and rapidly translocates to the nucleus. Within the nucleus, the GR either induces gene transcription by binding to specific deoxyribonucleic acid elements in the promoter/enhancer regions of responsive genes or reduces gene transcription by transrepression. The GR reduces gene transcription by interaction with pro-inflammatory transcription factors such as activation protein-1 and nuclear factor-kappa B. These effects of the GR on gene expression involve changes in the chromatin structure localized to the promoter sites of responsive genes. Many of the detrimental side-effects of corticosteroids are believed to be due to gene induction, leading to the search for novel corticosteroids which can repress inflammatory genes without inducing gene transcription.
  • Journal article
    Ober C, Moffatt MF, 2000,

    Contributing factors to the pathobiology. The genetics of asthma.

    , Clin Chest Med, Vol: 21, Pages: 245-261, ISSN: 0272-5231

    Markers in 19 chromosomal regions have shown some evidence of linkage to asthma, atopy, or related phenotypes in multiple independent genome-wide searches. Linkages to five of these regions (5q, 6p, 11q, 12q, and 13q) have also been reported in non-genome-wide screens. In addition, at least two independent studies have reported linkages to markers on 16p. Numerous candidate genes in these regions have shown varying levels of association to asthma or atopic phenotypes, potentially implicating them as disease susceptibility loci. These include the IL4, CD14, and B2ADR genes on 5q, the HLA-DRB1 and TNF genes on 6p, the FCERB1 and CC16 genes on 11q, and the IL4RA gene on 16p. It still remains to be determined whether polymorphisms in these genes account for the reported linkages in these regions. Studies are underway in laboratories around the world to identify the disease-causing variations in these genes that account for the linkages just discussed. Identifying specific genetic polymorphisms that influence asthma and atopic phenotypes will shed light on the molecular pathways involved in these complex disorders and provide a better understanding of the pathophysiology of asthma and atopy.
  • Journal article
    Palmer LJ, Burton PR, Faux JA, James AL, Musk AW, Cookson WOet al., 2000,

    Independent inheritance of serum immunoglobulin E concentrations and airway responsiveness.

    , Am J Respir Crit Care Med, Vol: 161, Pages: 1836-1843, ISSN: 1073-449X

    Elevated serum Immunoglobulin E (IgE) levels and increased airway responsiveness (AR) are correlated traits that are characteristic of asthma. It is not known to what extent these traits arise from distinct or shared genetic determinants. We investigated the genetic and environmental components of variance of serum total and specific IgE levels and AR in an Australian population-based sample of 232 Caucasian nuclear families. The inter-relationships of the genetic determinants of these traits were also investigated. Log(e) total serum IgE levels had a narrow-sense heritability (h(2)(N)) of 47.3% (SE = 10.0%). Specific serum IgE levels against house dust mite and timothy grass, measured as a RAST Index, ad a h(2)(N) of 33.8% (SE = 7.3%). AR, quantified by the log(e) dose-response slope to methacholine (DRS), had a h(2)(N) of 30.0% (SE = 12.3%). Extended modeling demonstrated an approximate 70% overlap in the genetic determinants of total and specific serum IgE levels. The genetic determinants of serum IgE levels and AR exhibited less than 30% sharing. These data are consistent with the existence of multiple genetic determinants of the pathophysiologic traits associated with asthma, and suggest that AR is genetically distinct from atopy. These results have implications for gene discovery programs.
  • Journal article
    Brown JS, Aufauvre-Brown A, Brown J, Jennings JM, Arst H, Holden DWet al., 2000,

    Signature-tagged and directed mutagenesis identify PABA synthetase as essential for <i>Aspergillus fumigatus</i> pathogenicity

    , MOLECULAR MICROBIOLOGY, Vol: 36, Pages: 1371-1380, ISSN: 0950-382X
    • Cite
    • Citations: 115
  • Journal article
    Davies J, Neth O, Alton E, Klein N, Turner Met al., 2000,

    Differential binding of mannose-binding lectin to respiratory pathogens in cystic fibrosis

    , LANCET, Vol: 355, Pages: 1885-1886, ISSN: 0140-6736
  • Journal article
    Espeso EA, Roncal T, Díez E, Rainbow L, Bignell E, Alvaro J, Suárez T, Denison SH, Tilburn J, Arst HN, Peñalva MAet al., 2000,

    On how a transcription factor can avoid its proteolytic activation in the absence of signal transduction

    , EMBO JOURNAL, Vol: 19, Pages: 2391-2391, ISSN: 0261-4189
  • Journal article
    Chabat F, Hansell DM, Yang GZ, 2000,

    Gradient correction and classification of CT lung images for the automated quantification of mosaic attenuation pattern?

    , Journal of Computer Assisted Tomography, Vol: 24, Pages: 437-447
  • Journal article
    Espeso EA, Arst HN, 2000,

    On the mechanism by which alkaline pH prevents expression of an acid-expressed gene

    , MOLECULAR AND CELLULAR BIOLOGY, Vol: 20, Pages: 3355-3363, ISSN: 0270-7306

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