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Liz Allen

Dr Elizabeth Allen BSC, PhD, DipRCPath

Senior Lecturer in Biomedical Science

Summary

I studied for a BSc degree in Biochemistry at Bath University, followed by a PhD in Virology from Glasgow University and post-doctoral positions in research institutions in Glasgow and London. My research work was focused on transcription factor activation of gene expression in viral systems and cancer.

I then moved to the pharmaceutical industry, where I was involved in identifying genes from the human genome sequence which were suitable candidates for drug development. Since 2007 I have been working as a HCPC registered Clinical Scientist in diagnostic genetics in the NHS. I have worked in a number of clinical areas, ranging from haemostasis to metabolic disorders.

I was appointed as a lecturer at Sheffield Hallam University in May 2015.

  • About

    I studied for a BSc degree in Biochemistry at Bath University, followed by a PhD in Virology from Glasgow University. My PhD project investigated how viral proteins activate gene transcription. I continued my research work investigating how transcription factors activate gene expression in cancer, working as a post-doctoral research associate at institutions in Glasgow and London.

    I then moved to the pharmaceutical industry, working for three different pharmaceutical and biotech companies. The human genome sequencing project had just been completed. I was involved in several research projects trying to discover previously unidentified genes from the human genome sequence, which would be suitable targets for drug development.

    Since 2007 I have been working as a HCPC registered Clinical Scientist in diagnostic genetics in the NHS, firstly in Manchester and more recently at Sheffield Children's Hospital. I have worked in a number of clinical areas, ranging from haemostasis to metabolic disorders. I was appointed as a lecturer at Sheffield Hallam University in May 2015, and I am teaching several subjects in biomedical sciences, including clinical chemistry, blood sciences, cancer and biology of disease.

    Investigation of the molecular mechanisms of Vanishing White Matter disease
    Investigation of epigenetic mechanisms controlling gene transcription.

  • Teaching

  • Research

    Characterisation of the importance of eIF2B bodies in CACH/VWM disease

    The initiation phase of protein synthesis is a key regulatory step in gene expression. One of the major control points in the translation initiation pathway is catalysed by the guanine nucleotide exchange factor eIF2B. In recent years a fatal human disease known as leukoencephalopathy with vanishing white matter (VWM) has been linked to mutations in all five subunits of eIF2B. The mechanism of pathogenesis of VWM is not clearly understood. The pathophysiology of VWM shows a central role for glial cells in the disease mechanism; however why oligodendrocytes and astrocytes are more affected than other cell types when eIF2B is required for all protein synthesis is unknown.

    The key regulatory complex eIF2B and the G protein eIF2 co-localise to a specific cytoplasmic focus, termed eIF2B bodies. These bodies represent sites where the activity of eIF2B is controlled and regulated. This suggests that eIF2B bodies play an important role during active translation. We have recently identified a discrete localisation pattern for eIF2B subunits in glial cells. The effect of VWM mutations on the formation of these bodies in glial cells will be investigated to determine their functional impact.

    We will use microscopy techniques such as FRET and FRAP to analyse eIF2B complexes.

    Determination of the translational profile of VWM mutants in glial cells

    Ribosome profiling is a method based on deep sequencing of ribosome-protected mRNA fragments. This allows the identification and quantification of the RNA molecules which are being actively translated within a cell. We aim to use CRISPR-cas9 technology to introduce mutant forms of the eIF2B subunits into glial cells. These cells will then be analysed using ribosome profiling, in order to determine the translational profile of glial cells in the presence and absence of common VWM mutations. This may highlight additional pathways underlying the mechanism of disease in these cells.

    Dr L Crookes, Sheffield Diagnostic Genetics Service, Sheffield Children's NHS Foundation Trust

  • Publications

    Coffey AJ, Durkie M, Hague S, McLay K, Emmerson J, Lo C, Klaffke S, Joyce CJ, Dhawan A, Hadzic N, Mieli-Vergani G, Kirk R, Elizabeth Allen K, Nicholl D, Wong S, Griffiths W, Smithson S, Giffin N, Taha A, Connolly S, Gillett GT, Tanner S, Bonham J, Sharrack B, Palotie A, Rattray M, Dalton A, Bandmann O. (2013) A genetic study of Wilson's disease in the United Kingdom. Brain 136(Pt 5):1476-87. doi: 10.1093/brain/awt035.

    Searle C, Andresen BS, Wraith E, Higgs J, Gray D, Mills A, Allen KE, Hobson E. (2013) A large intragenic deletion in the ACADM gene can cause MCAD deficiency but is not detected on routine sequencing. JIMD Rep. 11:13-6. doi: 10.1007/8904_2013_216.

    Temple R, Allen E, Fordham J, Phipps S, Schneider HC, Lindauer K, Hayes I, Lockey J, Pollock K, Jupp R. (2001) Microarray analysis of eosinophils reveals a number of candidate survival and apoptosis genes. Am J Respir Cell Mol Biol. 25(4): 425-33.

    Morris, L., Allen, K. E. and La Thangue, N. B. (2000) Regulation of E2F transcription by cyclinE/cdk2 kinase mediated through p300/CBP coactivators. Nature Cell Biol. 2(4):232-9.

    De la Luna, S., Allen, K. E., Mason, S. L. and La Thangue, N. B. (1999) Integration of a growth-suppressing BTB/POZ domain protein with the DP component of the E2F transcription factor. EMBO J.18(1) 121-28.

    May, G. H. W., Allen, K. E., Clark, W. and Gillespie, D. A. F. (1998) Analysis of the interaction between c-Jun and c-Jun N-terminal Kinase in vivo. J. Biol. Chem. 273(50) 33429-35.

    Allen, K. E., de la Luna, S., Kerkhoven, R., Bernards, R. and La Thangue, N. B. (1997) Distinct mechanisms of nuclear accumulation regulate the functional consequences of E2F transcription factors. J. Cell Sci. 110, 2819-2831.

    Allen, K. E. and Everett, R. D. (1997). Mutations which alter the DNA binding properties of the herpes simplex virus type 1 transactivating protein Vmw175 also affect its ability to support viral replication. J. Gen. Virol. 78, 2913-2922.

    Buck, V., Allen, K. E., Sorensen, T., Bybee, A., Hijmans, E. M., Voorhoeve, P. M., Bernards, R. and La Thangue, N. B. (1995). Molecular and functional characterisation of E2F-5, a new member of the E2F family. Oncogene 11, 31-38.

    Tyler, J. K., Allen, K. E. and Everett, R. D. (1994). Mutation of a single lysine residue severely impairs the DNA recognition and regulatory functions of the VZV gene 62 transactivator protein. Nucleic Acids Res., 22, 270-278.

  • Post graduate supervision

    Co-supervisor - Characterisation of the importance of eIF2B bodies in CACH/VWM disease and determination of the translational profile of VWM mutants in glial cells.

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