Professor Steve Jackson - Associate Faculty

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.

Steve graduated from Leeds University in 1983 and then carried out his PhD research working with Jean Beggs on yeast RNA splicing at Imperial College, London and Edinburgh University, gaining his PhD in 1987.

Steve moved to the USA to carry out his postdoctoral research with Robert Tjian at Berkeley, where he developed an interest in the regulation of transcription. He returned to the UK in 1991 to become a Junior Group Leader at the then Wellcome-CRC Institute to continue his research into transcription by eukaryotic RNA polymerases II and III. This work was subsequently expanded to include the transcriptional apparatus in Archaea.

Through characterising the functions of the DNA-dependent protein kinase, Steve was led into the field of DNA repair and DNA-damage signalling. Although a considerable amount of his lab's current work is still focused on pathways controlled by DNA-PK and the related kinases ATM and ATR, his research is increasingly determining how other post-translational modifications, such as protein acetylation, poly(ADP)-ribosylation, ubiquitylation and sumoylation, also control key DDR events.

In 1997 Steve founded KuDOS Pharmaceuticals with the aim of translating knowledge of DDR pathways into new treatments for cancer. KuDOS developed into a fully integrated drug-discovery and drug-development company, being acquired by AstraZeneca in 2005. KuDOS drugs are now being evaluated in a number of clinical trials.

Recently, Steve founded MISSION Therapeutics Ltd with the aim is to translate new molecular understandings of human cell biology into drugs that will markedly improve the management of life-threatening diseases, particularly cancer.

Selected Publications

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

    Rodriguez R, Miller KM, Forment JV, Bradshaw CR, Nikan M, Britton S, Oelschlaegel T, Xhemalce B, Balasubramanian S and Jackson SP

    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, Rusch A, Thomas A, Blundred R, Smith P, Kzhyshkowska J, Dobner T, Taylor AM, Turnell AS, Stewart GS, Grand RJ and Jackson SP

    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, Bartek J, Baer R, Lukas J and Jackson SP

    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, Von Zglinicki T, Saretzki G, Carter NP and Jackson SP

    Nature 2003;426;6963;194-8

* quick link - http://q.sanger.ac.uk/o84o8qfa