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Biomedical subjects

Andrew Fraser

Publications and source records attributed to Andrew Fraser.

5 recordsLinked to original sources
PubMed2003

Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans.

Ageing is a fundamental, unsolved mystery in biology. DAF-16, a FOXO-family transcription factor, influences the rate of ageing of Caenorhabditis elegans in response to insulin/insulin-like growth factor 1 (IGF-I) signalling. Using DNA microarray analysis, we have found that DAF-16 affects expression of a set of genes during early adulthood, the time at which this pathway is known to control ageing. Here we find that many of these genes influence the ageing process. The insulin/IGF-I pathway functions cell non-autonomously to regulate lifespan, and our findings suggest that it signals other cells, at least in part, by feedback regulation of an insulin/IGF-I homologue. Furthermore, our findings suggest that the insulin/IGF-I pathway ultimately exerts its effect on lifespan by upregulating a wide variety of genes, including cellular stress-response, antimicrobial and metabolic genes, and by downregulating specific life-shortening genes.

Aging↗
PubMed2003

Worms in L.A.

Explore the source record for details and available documents.

Animals↗
PubMed2003

Phenotypic differences between peripheral myelin protein-22 (PMP22) and myelin protein zero (P0) mutations associated with Charcot-Marie-Tooth-related diseases.

Mutations in the genes for peripheral myelin protein-22 (PMP22) and myelin protein zero (P0) cause human hereditary neuropathies with varying clinical and pathological phenotypes. In this study, we examine the effects of representative disease-causing mutations on the subcellular distribution of their corresponding PMP22- and P0-enhanced green fluorescent protein (EGFP) fusion proteins. In transiently transfected HeLa and 293 cells, we find that wild-type P0-EGFP and PMP22-EGFP are efficiently synthesized and transported through the secretory pathway to the plasma membrane. The P0-EGFP and PMP22-EGFP mutants can be classified into several groups: those that are transported to the plasma membrane as in the majority of P0 mutants; those that are retained in the endoplasmic reticulum as in the majority of PMP22 mutants; and those that are a mixture of the two. In addition, several of these disease-causing mutations are associated with the development of abnormal intracellular cytoplasmic structures that we have previously identified as either intracellular myelin figures or aggresomes. Our studies indicate that different types of PMP22 and P0 mutations are associated with specific intracellular chaperone proteins, including calnexin and BiP, and that these associations can be altered by glycosylation. These findings indicate that the various P0 and PMP22 mutants may exert their pathogenic effects in different subcellular compartments and by different mechanisms in the mammalian cell.

Cell Compartmentation↗
PubMed2003

Privacy and the secondary use of data in health research in Scotland.

In response to new data protection legislation for the UK and widespread concern about its implications, the Scottish Executive set up the Confidentiality and Security Advisory Group for Scotland (CSAGS) to place the use of personal health information in a modern setting. The group affirmed the principle of consent and, more broadly, the importance of involving patients and the public in decisions about their health information. It promoted methods of acceptable anonymisation of data, and the need for good stewardship and disclosure of data uses to the greatest extent possible, where explicit individual consent and anonymisation were not practicable. They did not recommend pursuit of legislation, preferring consensus, informed debate and widespread acceptance of the proposed arrangements. The Scottish Executive is now responding to the work of CSAGS to develop systems that command public and patient confidence, promote good practice for clinicians and researchers, and preserve important public health and research functions.

Access to Information↗