A C Lloyd

Summary

Affiliation: University College London
Country: UK

Publications

  1. doi request reprint The regulation of cell size
    Alison C Lloyd
    MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, Gower Street, London WC1E 6BT, UK Electronic address
    Cell 154:1194-205. 2013
  2. ncbi request reprint Ras versus cyclin-dependent kinase inhibitors
    A C Lloyd
    MRC Laboratory for Molecular Cell Biology, University College London, London, UK
    Curr Opin Genet Dev 8:43-8. 1998
  3. pmc Distinct functions for ERKs?
    Alison C Lloyd
    MRC Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK
    J Biol 5:13. 2006
  4. ncbi request reprint Limits to lifespan
    Alison C Lloyd
    Cancer Research Campaign, MRC Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK
    Nat Cell Biol 4:E25-7. 2002
  5. ncbi request reprint Lack of replicative senescence in normal rodent glia
    N F Mathon
    MRC Laboratory for Molecular Cell Biology, University College London, Gower Street, London WC1E 6BT, UK
    Science 291:872-5. 2001
  6. ncbi request reprint Cooperating oncogenes converge to regulate cyclin/cdk complexes
    A C Lloyd
    Imperial Cancer Research Fund ICRF, London, UK
    Genes Dev 11:663-77. 1997
  7. ncbi request reprint Lack of replicative senescence in cultured rat oligodendrocyte precursor cells
    D G Tang
    MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK
    Science 291:868-71. 2001
  8. ncbi request reprint Cell senescence and cancer
    N F Mathon
    Department of Biochemistry, University College London, UK
    Nat Rev Cancer 1:203-13. 2001
  9. pmc The Ras/Raf/ERK signalling pathway drives Schwann cell dedifferentiation
    Marie C Harrisingh
    MRC Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, London, UK
    EMBO J 23:3061-71. 2004
  10. ncbi request reprint Hijacking the ERK signaling pathway: Mycobacterium leprae shuns MEK to drive the proliferation of infected Schwann cells
    Luke A Noon
    Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK
    Sci STKE 2005:pe52. 2005

Collaborators

  • L Cheng
  • D G Tang
  • David B Parkinson
  • Pedro Echave
  • Luke A Noon
  • Marie C Harrisingh
  • N F Mathon
  • Simona Parrinello
  • Daniel Rubio
  • Elena Perez-Nadales
  • Denise S Malcolm
  • Philip J Mitchell
  • Masanori Nakayama
  • Ralf H Adams
  • Patrick Wingfield Digby
  • Sara Ribeiro
  • Ilaria Napoli
  • Robin D S Doddrell
  • Marina Fedorova
  • Michael R Duchen
  • Jake Jacobson
  • Gisela Machado-da-Silva
  • Rebecca S Arkell
  • Richard Mitter
  • Ian J Conlon
  • Ricardo de la Fuente
  • Juan C Cigudosa
  • Javier Garcia-Castro
  • Antonio Bernad
  • Maria C Martin
  • Anne W Mudge
  • D S Malcolm
  • M C Harrisingh

Detail Information

Publications17

  1. doi request reprint The regulation of cell size
    Alison C Lloyd
    MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, Gower Street, London WC1E 6BT, UK Electronic address
    Cell 154:1194-205. 2013
    ..This Review will discuss our current understanding of how a cell sets its size, how it can adapt its size to a changing environment, and how these processes are relevant to human disease. ..
  2. ncbi request reprint Ras versus cyclin-dependent kinase inhibitors
    A C Lloyd
    MRC Laboratory for Molecular Cell Biology, University College London, London, UK
    Curr Opin Genet Dev 8:43-8. 1998
    ..In the absence of a negative growth signal from Ras, such as in most immortalised cell lines, Ras acts positively on the cell cycle. Insights have been made into the mechanisms by which Ras abrogates remaining cell-cycle controls...
  3. pmc Distinct functions for ERKs?
    Alison C Lloyd
    MRC Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK
    J Biol 5:13. 2006
    ..Recent studies add complexity to this cascade by indicating that the two ERK kinases, ERK1 (p44ERK1) and ERK2 (p42ERK2), may have distinct functions...
  4. ncbi request reprint Limits to lifespan
    Alison C Lloyd
    Cancer Research Campaign, MRC Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK
    Nat Cell Biol 4:E25-7. 2002
    ..Recent work has now challenged this view by demonstrating that extrinsic factors might be determining proliferative potential...
  5. ncbi request reprint Lack of replicative senescence in normal rodent glia
    N F Mathon
    MRC Laboratory for Molecular Cell Biology, University College London, Gower Street, London WC1E 6BT, UK
    Science 291:872-5. 2001
    ..These findings demonstrate that senescence is not an inevitable consequence of extended proliferation in culture...
  6. ncbi request reprint Cooperating oncogenes converge to regulate cyclin/cdk complexes
    A C Lloyd
    Imperial Cancer Research Fund ICRF, London, UK
    Genes Dev 11:663-77. 1997
    ..Thus, signaling by Raf and its cooperating partners converges at the regulation of cyclin/cdk complexes, with the cellular responses to Raf modulated by p53...
  7. ncbi request reprint Lack of replicative senescence in cultured rat oligodendrocyte precursor cells
    D G Tang
    MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK
    Science 291:868-71. 2001
    ..Our findings suggest that some normal rodent precursor cells have an unlimited proliferative capacity if cultured in conditions that avoid both differentiation and the activation of checkpoint responses that arrest the cell cycle...
  8. ncbi request reprint Cell senescence and cancer
    N F Mathon
    Department of Biochemistry, University College London, UK
    Nat Rev Cancer 1:203-13. 2001
    ..In this review, we discuss the pathways of cell senescence, the mechanisms involved and the role that these pathways have in regulating the initiation and progression of cancer...
  9. pmc The Ras/Raf/ERK signalling pathway drives Schwann cell dedifferentiation
    Marie C Harrisingh
    MRC Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, London, UK
    EMBO J 23:3061-71. 2004
    ..Our results suggest that the effects of Ras signalling on the differentiation state of Schwann cells may be important in the pathogenesis of these tumours...
  10. ncbi request reprint Hijacking the ERK signaling pathway: Mycobacterium leprae shuns MEK to drive the proliferation of infected Schwann cells
    Luke A Noon
    Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK
    Sci STKE 2005:pe52. 2005
    ..In this Perspective, we discuss this important piece of work and highlight the noncanonical pathway used by M. leprae to induce proliferation...
  11. ncbi request reprint Cell size regulation in mammalian cells
    Pedro Echave
    MRC Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, London, UK
    Cell Cycle 6:218-24. 2007
    ..This has profound effects on cell behaviour...
  12. doi request reprint EphB signaling directs peripheral nerve regeneration through Sox2-dependent Schwann cell sorting
    Simona Parrinello
    MRC Laboratory for Molecular Cell Biology and the UCL Cancer Institute, University College London, Gower Street, London WC1E 6BT, UK
    Cell 143:145-55. 2010
    ..Our results identify a link between Ephs and Sox proteins, providing a mechanism by which progenitor cells can translate environmental cues to orchestrate the formation of new tissue...
  13. pmc Extracellular growth factors and mitogens cooperate to drive mitochondrial biogenesis
    Pedro Echave
    MRC Laboratory for Molecular Cell Biology, The Cancer Institute, University College London, London, UK
    J Cell Sci 122:4516-25. 2009
    ..This separation of the pathways that drive mitochondrial biogenesis and cell growth provides a mechanism for the modulation of mitochondrial density according to the metabolic requirements of the cell...
  14. ncbi request reprint Treating leprosy: an Erb-al remedy?
    Luke A Noon
    MRC Laboratory for Molecular Cell Biology and the Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, UK
    Trends Pharmacol Sci 28:103-5. 2007
    ..These findings have relevance for the potential treatment of leprosy and they highlight parallels between the dedifferentiation signal in leprosy and that in nerve injury and cancer...
  15. pmc Dissecting the contribution of p16(INK4A) and the Rb family to the Ras transformed phenotype
    Philip J Mitchell
    MRC Laboratory for Molecular Cell Biology and Department of Biochemistry, University College London, London WC1E 6BT, United Kingdom
    Mol Cell Biol 23:2530-42. 2003
    ..We demonstrate here a role for p16(INK4A) in the loss of cell cycle controls required for tumorigenesis and show how accumulating genetic changes cooperate and contribute to the transformed phenotype...
  16. ncbi request reprint Ras/Raf/ERK signalling and NF1
    Marie C Harrisingh
    MRC Laboratory for Molecular Cell Biology and the Department of Biochemistry, University College London, Gower Street, London, UK
    Cell Cycle 3:1255-8. 2004
    ..We have found that Ras/Raf/ERK signalling can drive the de-differentiation of myelinated Schwann cells. In this review, we discuss how our results may contribute to the understanding of tumor formation in NF1 patients...
  17. ncbi request reprint Spontaneous human adult stem cell transformation
    Daniel Rubio
    Department of Immunology and Oncology, Centro Nacional de Biotecnología Consejo Superior de Investigaciones Científicas, UAM Campus de Cantoblanco, Darwin, 3 E 28049 Madrid, Spain
    Cancer Res 65:3035-9. 2005
    ..Our findings indicate the importance of biosafety studies of mesenchymal stem cell biology to efficiently exploit their full clinical therapeutic potential...