Dr Sarah AllinsonSenior Lecturer
Dr Allinson's work is aimed at gaining a better understanding of how cells respond to DNA damage. The two main areas of her research are (i) understanding how skin cells respond to damage caused by ultraviolet radiation and (ii) the mechanisms underlying the repair of breaks in the DNA backbone and factors that might affect their efficiency.
Cellular DNA is inherently unstable and is continually undergoing damage and degradation. Such damage can be caused by exposure to environmental carcinogens and also as a consequence of normal cellular metabolism, for example via the production of reactive oxygen species (ROS). My research is aimed at understanding the cellular response to DNA damage, with particular emphasis on the base excision repair (BER) and single strand break repair (SSBR) pathways.
Understanding how DNA repair is regulated at the level of single repair events and also within the cell as a whole can aid our understanding of inter-individual variation in cancer susceptibility and hopefully provide clues as to how repair in tumour cells may be attenuated to render cancer treatments more effective. With this aim in mind, there are a number of projects currently in progress in my lab.
Mechanistic studies of DNA repair
DNA repair pathways are multi-step processes involving a number of different enzymes and a network of protein-protein interactions. My research on DNA repair is aimed at understanding how the BER and SSBR pathways are co-ordinated and also how their efficiency might be affected by environmental carcinogens such as heavy metals. Through the detailed characterisation of repair of model DNA substrates by purified recombinant enzymes and cell extracts, facilitated by techniques such as site-directed mutagenesis, siRNA and protein-DNA interaction assays, we aim to gain a new mechanistic insight into how damaged DNA is repaired in vivo.
The cellular response to UVA exposure
We are currently investigating the effects of UVA exposure on human cells. Originally thought not to be a significant risk factor for skin cancer, UVA is now believed to contribute as much as 10-20% of the cancer-causing dose of sunlight. UVA induces DNA damage indirectly via photosensitiser-mediated production of ROS. One area of research that we are currently actively pursuing involves characterising the effects of UVA on stress response pathways and seeing how they differ from those induced by shorter wavelength UVB.
Work in my laboratory is currently funded by the BBSRC, Boots UK Limited and the Dowager Countess Eleanor Peel Trust.
BIOL437 Molecular Basis of Cancer: Module organiser and delivery of lectures/workshops etcBIOL463 Cell Biology Research Skills: Delivery of practical on flow cytometryBIOL353 Cancer: Module organiser and delivery of lectures/workshops/practicals etcBIOL253 Genetics: Delivery of lectures/workshops/practicals etc
BIOL272 Cell Biology Techniques: Delivery of two lecturesSpecial Study Module convenor on the Medicine MBChB degree
PhD Supervision Interests
I can offer PhD and MSc research projects on either molecular mechanisms of eukaryotic DNA repair or biological effects of ultraviolet radiation/skin cancer. Please contact me for further details (No funded positions currently available)
Platinum trimethyl bipyridyl thiolates – new, tunable, red- to near IR emitting luminophores for bioimaging applications
Steel, H., Allinson, S., Andre, J., Coogan, M., Platts, J.A. 1/07/2015 In: Chemical Communications. 51, 57, p. 11441-11444. 4 p.
Characterisation of the p53-Mediated Cellular Responses Evoked in Primary Mouse Cells Following Exposure to Ultraviolet Radiation
McFeat, G., Allinson, S., McMillan, T. 30/09/2013 In: PLoS ONE. 8, 9, 9 p.
Timeframes of UVA-induced bystander effects in human keratinocytes.
Whiteside, J.R., Allinson, S.L., McMillan, T.J. 03/2011 In: Photochemistry and Photobiology. 87, 2, p. 435-440. 6 p.
Cadmium and copper inhibit both DNA repair activities of polynucleotide kinase.
Whiteside, J.R., Box, C.L., McMillan, T.J., Allinson, S.L. 01/2010 In: DNA Repair. 9, 1, p. 83-89. 7 p.
DNA end-processing enzyme polynucleotide kinase as a potential target in the treatment of cancer
Allinson, S. 2010 In: Future Oncology. 6, 6, p. 1031-1042. 12 p.
Cellular and sub-cellular responses to UVA in relation to carcinogenesis
Ridley, A.J., Whiteside, J.R., McMillan, T.J., Allinson, S.L. 2009 In: International Journal of Radiation Biology. 85, 3, p. 177-195. 19 p.
Targeted cornea limbal stem/progenitor cell transfection in an organ culture model
Zhao, B., Allinson, S.L., Ma, A., Bentley, A.J., Martin, F.L., Fullwood, N.J. 08/2008 In: Investigative Ophthalmology and Visual Science. 49, 8, p. 3395-3401. 7 p.
CHIP-Mediated Degradation and DNA Damage-Dependent Stabilization Regulate Base Excision Repair Proteins.
Parsons, J.L., Tait, P.S., Finch, D., Dianova, I.I., Allinson, S.L., Dianov, G.L. 29/02/2008 In: Molecular Cell. 29, 4, p. 477-487. 11 p.
Ectopic overexpression of theta class glutathione transferases in a human keratinocyte cell line.
Jackson, K.M., Allinson, S.L., McMillan, T.J. 11/2007 In: Mutagenesis. 22, 6, p. 444-445. 2 p.
Growth kinetics in MCF-7 cells modulate benzo[a]pyrene-induced CYP1A1 up-regulation.
Jiao, H., Allinson, S.L., Walsh, M.J., Hewitt, R., Cole, K.J., Phillips, D.H., Martin, F.L. 03/2007 In: Mutagenesis. 22, 2, p. 111-116. 6 p.
The phosphatase activity of mammalian polynucleotide kinase takes precedence over its kinase activity repair of single strand breaks.
Dobson, C.J., Allinson, S.L. 05/2006 In: Nucleic Acids Research. 34, 8, p. 2230-2237. 8 p.
CYP1A1 up-regulation in MCF-7 cells following benzo[a]pyrene treatment occurs primarily during S-phase : a significant modulator of consequent genotoxicity.
Martin, F.L., Allinson, S.L., Walsh, M.J., Hewitt, R., Cole, K.J., Phillips, D.H., Jiao, H. 2006 In: European Journal of Genetic and Molecular Toxicology. 36
DNA base damage recognition and processing.
Dianov, G.L., Allinson, S.L. 2006 In: Genome dynamics and stability. Berlin : Springer p. 287-314. 28 p.
DNA polymerase Beta promotes recruitment of XRCC1-Ligase III alpha to sites of base excision repair.
Parsons, J.L., Dianova, I.I., Allinson, S.L., Dianov, G.L. 9/08/2005 In: Biochemistry. 44, 31, p. 10613-10619. 7 p.
Poly(ADP-ribose) polymerase-1 protects excessive DNA strand breaks from deterioration during repair in human cell extracts.
Parsons, J.L., Dianova, I.I., Allinson, S.L., Dianov, G.L. 04/2005 In: FEBS Journal. 272, 8, p. 2012-2021. 10 p.
XRCC1–DNA polymerase ß interaction is required for efficient base excision repair.
Sleeth, K.M., Dianova, I.I., Allinson, S.L., Parsons, J.L., Breslin, C., Caldecott, K.W., Dianov, G.L. 04/2004 In: Nucleic Acids Research. 32, 8, p. 2550-2555. 6 p.
Orchestration of base excision repair by controlling the rates of enzymatic activities.
Allinson, S.L., Sleeth, K.M., Matthewman, G.E., Dianov, G.L. 01/2004 In: DNA Repair. 3, 1, p. 23-31. 9 p.
Repair of abasic sites in DNA.
Dianov, G.L., Sleeth, K.M., Dianova, I.I., Allinson, S.L. 29/10/2003 In: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis. 531, 1-2, p. 157-163. 7 p.
Mammalian base excision repair.
Dianov, G.L., Allinson, S.L., Budworth, H., Sleeth, K.M. 2003 In: Eukaryotic DNA damage surveillance and repair. Amsterdam : Kluwer Academic Publishers
Poly(ADP-ribose) polymerase in base excision repair: always engaged, but not essential for DNA damage processing.
Allinson, S.L., Dianova, I.I., Dianov, G.L. 2003 In: Acta Biochimica Polonica. 50, 1, p. 169-179. 11 p.
Co-ordination of base excision repair.
Allinson, S.L., Dianov, G.L. 2002 In: Recent research development in repair and mutagenesis. Research Signpost
DNA polymerase B is the major dRP lyase involved in repair of oxidative base lesions in DNA by mammalian cell extracts
Allinson, S.L., Dianova, I.I., Dianov, G.L. 3/12/2001 In: EMBO Journal. 20, 23, p. 6919-6926. 8 p.
NWCR Summer Studentships 2018 and 2019
01/07/2018 → 30/09/2019
North West Cancer Research 'We need to talk about skin cancer' event
Public Lecture/ Debate/Seminar