Search Results - "Haughton, Michele F."

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  1. 1

    Telomerase prevents the accelerated cell ageing of Werner syndrome fibroblasts by Faragher, Richard G.A, Wyllie, Fiona S, Jones, Christopher J, Skinner, Julia W, Haughton, Michele F, Wallis, Corrin, Wynford-Thomas, David, Kipling, David

    Published in Nature genetics (01-01-2000)
    “…Werner syndrome (WS) is a rare disorder inherited in an autosomal recessive manner and characterized by accelerated ageing. WS fibroblasts display an…”
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  2. 2

    Prevention of Accelerated Cell Aging in the Werner Syndrome by DAVIS, TERENCE, HAUGHTON, MICHÈLE F., JONES, CHRISTOPHER J., KIPLING, DAVID

    Published in Annals of the New York Academy of Sciences (01-05-2006)
    “…:  In the Werner syndrome (WS) fibroblasts have an increased life span and growth rate when treated with the p38 inhibitor SB203580. Additionally, the cellular…”
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  3. 3

    Prevention of Accelerated Cell Aging in Werner Syndrome Using a p38 Mitogen-Activated Protein Kinase Inhibitor by Davis, Terence, Baird, Duncan M., Haughton, Michèle F., Jones, Christopher J., Kipling, David

    “…We investigated the role of p38 mitogen-activated protein kinase (MAPK) signalling in the accelerated aging of Werner Syndrome (WS) fibroblasts by use of…”
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  4. 4

    Telomere-based proliferative lifespan barriers in Werner-syndrome fibroblasts involve both p53-dependent and p53-independent mechanisms by Davis, Terence, Singhrao, Sim K, Wyllie, Fiona S, Haughton, Michele F, Smith, Paul J, Wiltshire, Marie, Wynford-Thomas, David, Jones, Christopher J, Faragher, Richard G A, Kipling, David

    Published in Journal of cell science (01-04-2003)
    “…Werner-syndrome fibroblasts have a reduced in vitro life span before entering replicative senescence. Although this has been thought to be causal in the…”
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  5. 5

    Telomere erosion triggers growth arrest but not cell death in human cancer cells retaining wild-type p53: implications for antitelomerase therapy by PRETO, Ana, SINGHRAO, Sim K, HAUGHTON, Michele F, KIPLING, David, WYNFORD-THOMAS, David, JONES, Christopher J

    Published in Oncogene (20-05-2004)
    “…Telomerase activity in tumours is often associated with p53 mutation. Many antitelomerase therapies take advantage of the inability of cells expressing mutant…”
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  6. 6

    Opposing effects of mutant ras oncoprotein on human fibroblast and epithelial cell proliferation: implications for models of human tumorigenesis by SKINNER, Julia, BOUNACER, Ali, BOND, Jane A, HAUGHTON, Michele F, DEMICCO, Catherine, WYNFORD-THOMAS, David

    Published in Oncogene (05-08-2004)
    “…Using microinjection of recombinant protein to directly control 'expression' levels, we have compared the proliferative response to ras oncogene activation in…”
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    Mutant p53 rescues human diploid cells from senescence without inhibiting the induction of SDI1/WAF1 by Bond, J A, Blaydes, J P, Rowson, J, Haughton, M F, Smith, J R, Wynford-Thomas, D, Wyllie, F S

    Published in Cancer research (Chicago, Ill.) (01-06-1995)
    “…Although the cyclin-dependent kinase inhibitor p21SDI1 (WAF1/CIP1) has been proposed as the mediator of p53-induced cell cycle arrest following DNA damage,…”
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  11. 11

    Dissociation of Telomere Dynamics from Telomerase Activity in Human Thyroid Cancer Cells by Jones, Christopher J., Soley, Anne, Skinner, Julia W., Gupta, Jyothi, Haughton, Michele F., Wyllie, Fiona S., Schlumberger, M., Bacchetti, Silvia, Wynford-Thomas, David

    Published in Experimental cell research (01-05-1998)
    “…Prevention of telomere erosion through acquisition of telomerase activity is thought to be an essential mechanism in most human cancer cells for avoidance of…”
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  12. 12

    S phase cell-cycle arrest following DNA damage is independent of the p53/p21(WAF1) signalling pathway by Wyllie, F S, Haughton, M F, Bond, J A, Rowson, J M, Jones, C J, Wynford-Thomas, D

    Published in Oncogene (07-03-1996)
    “…It is now likely that the cyclin-kinase inhibitor, p21(WAF1/SD11), is a key effector of p53-mediated cell-cycle arrest at the G(1)/S checkpoint following DNA…”
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