People

No image available
Professor Steve Jackson, FRS, FMedSci
Group Leader

Steve Jackson's research group focuses on understanding how cells detect and repair DNA damage via the activities of the 'DNA-damage response' (DDR). The importance of the DDR for maintaining good health is shown by the diseases that are associated with the alteration or loss of these activities; including neurodegenerative disease, immunodeficiency, premature ageing, infertility and cancer.

Research Programmes

Partners and Funders

Our research is drawing on the expertise and resources of the Sanger Institute. For example, to analyse mutations induced by DNA damage in wild-type and DDR-defective yeast strains we are collaborating with the Experimental cancer genetics project and the Cancer Genome Project. In addition, we will be working closely with the Cancer Genome Project to identify and develop new, molecularly targeted cancer therapies.
Internal Partners

Publications

  • Chemical inhibition of NAT10 corrects defects of laminopathic cells.

    Larrieu D, Britton S, Demir M, Rodriguez R and Jackson SP

    Science (New York, N.Y.) 2014;344;6183;527-32

  • A new method for high-resolution imaging of Ku foci to decipher mechanisms of DNA double-strand break repair.

    Britton S, Coates J and Jackson SP

    The Journal of cell biology 2013;202;3;579-95

  • KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling.

    Kaidi A and Jackson SP

    Nature 2013;498;7452;70-4

  • Regulation of DNA damage responses by ubiquitin and SUMO.

    Jackson SP and Durocher D

    Molecular cell 2013;49;5;795-807

  • RNF4, a SUMO-targeted ubiquitin E3 ligase, promotes DNA double-strand break repair.

    Galanty Y, Belotserkovskaya R, Coates J and Jackson SP

    Genes & development 2012;26;11;1179-95

  • Small-molecule-induced DNA damage identifies alternative DNA structures in human genes.

    Rodriguez R, Miller KM, Forment JV, Bradshaw CR, Nikan M et al.

    Nature chemical biology 2012;8;3;301-10

  • Regulation of DNA-end resection by hnRNPU-like proteins promotes DNA double-strand break signaling and repair.

    Polo SE, Blackford AN, Chapman JR, Baskcomb L, Gravel S et al.

    Molecular cell 2012;45;4;505-16

  • Dynamics of DNA damage response proteins at DNA breaks: a focus on protein modifications.

    Polo SE and Jackson SP

    Genes & development 2011;25;5;409-33

  • Human SIRT6 promotes DNA end resection through CtIP deacetylation.

    Kaidi A, Weinert BT, Choudhary C and Jackson SP

    Science (New York, N.Y.) 2010;329;5997;1348-53

  • Mammalian SUMO E3-ligases PIAS1 and PIAS4 promote responses to DNA double-strand breaks.

    Galanty Y, Belotserkovskaya R, Coates J, Polo S, Miller KM and Jackson SP

    Nature 2009;462;7275;935-9

  • The DNA-damage response in human biology and disease.

    Jackson SP and Bartek J

    Nature 2009;461;7267;1071-8

  • CDK targets Sae2 to control DNA-end resection and homologous recombination.

    Huertas P, Cortés-Ledesma F, Sartori AA, Aguilera A and Jackson SP

    Nature 2008;455;7213;689-92

  • Human CtIP promotes DNA end resection.

    Sartori AA, Lukas C, Coates J, Mistrik M, Fu S et al.

    Nature 2007;450;7169;509-14

  • XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining.

    Ahnesorg P, Smith P and Jackson SP

    Cell 2006;124;2;301-13

  • MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks.

    Stucki M, Clapperton JA, Mohammad D, Yaffe MB, Smerdon SJ and Jackson SP

    Cell 2005;123;7;1213-26

  • Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage.

    Falck J, Coates J and Jackson SP

    Nature 2005;434;7033;605-11

  • A DNA damage checkpoint response in telomere-initiated senescence.

    d'Adda di Fagagna F, Reaper PM, Clay-Farrace L, Fiegler H, Carr P et al.

    Nature 2003;426;6963;194-8