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, with the most advanced drug, olaparib, now being a registered drug worldwide for treating ovarian cancer.
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.
Synthetic viability genomic screening defines Sae2 function in DNA repair.
The EMBO journal 2015;34;11;1509-22
DNA repair. PAXX, a paralog of XRCC4 and XLF, interacts with Ku to promote DNA double-strand break repair.
Science (New York, N.Y.) 2015;347;6218;185-188
Systematic characterization of deubiquitylating enzymes for roles in maintaining genome integrity.
Nature cell biology 2014;16;10;1016-26, 1-8
Chemical inhibition of NAT10 corrects defects of laminopathic cells.
Science (New York, N.Y.) 2014;344;6183;527-32
KAT5 tyrosine phosphorylation couples chromatin sensing to ATM signalling.
Small-molecule-induced DNA damage identifies alternative DNA structures in human genes.
Nature chemical biology 2012;8;3;301-10
CDK targets Sae2 to control DNA-end resection and homologous recombination.
Mammalian SUMO E3-ligases PIAS1 and PIAS4 promote responses to DNA double-strand breaks.
Human CtIP promotes DNA end resection.
MDC1 directly binds phosphorylated histone H2AX to regulate cellular responses to DNA double-strand breaks.