Ralf H. Adams

After studying biochemistry at the University of Bayreuth, Ralf Adams started his research career at the Max-Planck-Institute for Brain Research and the Goethe University Frankfurt in Germany, where he obtained his Ph.D. in 1996. His work involved the cloning of new members of the semaphorin gene family and the characterization of their function in axon guidance.

Next, he moved to Rüdiger Klein's laboratory at the European Molecular Biology Laboratory in Heidelberg and began to work on the role of Eph/ephrin molecules in blood vessel morphogenesis. Together with his collaborator Angel Nebrada, he also investigated the function of the p38alpha mitogen-activated protein kinase.

In 2000, he became head of the Vascular Development Laboratory at the Cancer Research UK London Research Institute (formerly, Imperial Cancer Research Fund), where he and his laboratory made significant achievements by combining genetic approaches in the mouse with a wide range of cell and molecular biology methods. Several of their discoveries are directly relevant for human pathologies. For example, they were the first to show that the Eph receptor ligand ephrin-B1 controls skeletal morphogenesis and that defects in the human gene (EFNB1) lead to Craniofrontonasal Syndrome (CFNS). A different project has connected the cytoplasmic multi-PDZ domain protein GRIP1, an interaction partner of Eph/ephrin proteins and other molecules, with the rare but severe human congenital disease Fraser Syndrome. They also demonstrated that Junctional Adhesion Molecules (JAMs) are critical regulators of cell polarity.

Since he has moved as Director to the Max Planck Institute for Molecular Biomedicine and Professor the University of Münster in 2008, Ralf Adams and his group have continued to provide insight into key processes controlling developmental blood vessel growth and, in particular, its regulation by Notch, VEGF and Eph/ephrin signaling.

Julian Downward

Julian Downward obtained his bachelor's degree in Natural Sciences from Cambridge University and then studied for his Ph.D. in the laboratory of Michael Waterfield at the Imperial Cancer Research Fund in London, where he established in 1984 the link between a retroviral oncogene (v-erbB) and a cellular growth regulatory protein, the EGF receptor.

In 1986, he moved to Robert Weinberg's laboratory at the Whitehead Institute at the Massachusetts Institute of Technology in Cambridge, MA, where he began work on the role of Ras proteins in human cancer.

In 1989 he started his own lab at the Imperial Cancer Research Fund, now Cancer Research UK London Research Institute, where his lab has provided insights into the molecular mechanisms of function and regulation of oncogenic proteins of the Ras family and the importance of their mutational activation in human tumours.

In 2005 Julian was made a Fellow of the Royal Society, the UK's national academy of sciences, and became Associate Director of the Cancer Research UK London Research Institute.

Jan Hoeijmakers

Jan Hoeijmakers studied biology in Nijmegen. His PhD work on trypanosomes at the Univ. of Amsterdam resolved the molecular basis for antigenic variation by which trypanosomes switch each time surface coats and thereby escape from immune surveillance causing sleeping sickness.

In 1981 he joined the Dept. of Genetics of the Erasmus Univ. to work on DNA repair. He cloned the first of many subsequent human DNA-repair genes allowing elucidation of the reaction mechanism of nucleotide excision repair, discovered the strong evolutionary conservation of DNA repair, elucidated the basis of several enigmatic human repair syndromes, identified a new class of 'basal transcription disorders', generated a large number of DNA-repair mouse mutants that provided valuable insight into the complex etiology of human repair disorders and discovered a very strong, unanticipated link between DNA damage, repair and aging. Some of the repair mutants exhibit dramatically accelerated but bona fide aging limiting lifespan to only 3 weeks. Conditional mutants allowed targeting of accelerated aging to specific organs/stages of development (e.g. mouse mutants with dramatic aging only in the brain), making aging amenable to manipulation. Expression profiling revealed an unexpected similarity between short- and long-lived mice: both suppress the somatotrophic axis. This work led to the identification of a very important 'survival response' that promotes successful aging and counteracts cancer by redirecting energy from growth to defenses.

A new line of research explores the dynamic organization of DNA repair in living cells and intact organisms. His group generated the first mouse mutants with intrinsic defects in the biological clock. He owns several patents and discovered compounds that influence aging. His multi-disciplinary research has received several important awards.

In 2004 he started the 'DNage' whose mission is to provide solutions for medical/health problems associated with aging.

David Ish-Horowicz

Dr Ish-Horowicz gained his PhD at the MRC Laboratory of Molecular Biology in Cambridge on tRNA structure, and conducted postdoctoral work on Drosophila molecular genetics with Walter Gehring at the Biozentrum in Basel, Switzerland. He then established his own lab at the Imperial Cancer Research Fund (now Cancer Research UK), initially at their Mill Hill site, then in Oxford and, finally, at the main ICRF/CR-UK Lincoln's Inn Fields laboratory in London. He is currently a Professor of Cell and Developmental Biology at University College London and a Visiting Scientist in the Biochemistry Department, Oxford University.

Dr Ish-Horowicz's studies has driven major advances in understanding the molecular processes that generate different cell-types in developing animals, in both Drosophila and vertebrate model systems. His work identified the first metazoan corepressor, Groucho/TLE, which regulates transcription in response to many signalling pathways, including Notch and Wnt. He also showed how molecular motors transport selected mRNAs along microtubules to help target asymmetric protein production within cells. In vertebrates, he demonstrated that Notch intercellular signalling acts in the nervous system to maintain neuronal stem cells and, thereby, to generate neuronal diversity. He also provided the first evidence that a cyclic transcriptional oscillator acts during vertebrate segmentation in order to produce regular reiterated body-structures such as the axial skeleton. For these and other findings, he was awarded the 1997 Gulbenkian Science Prize and the 2007 Waddington Medal of the British Society of Developmental Biology, and was elected a Fellow of the Royal Society in 2002.

Klaus Rajewsky

Klaus Rajewsky developed a general method of targeted mutagenesis in mouse embryonic stem cells by introducing bacteriophage- and yeast-derived recombination systems, which opened the way for conditional gene targeting. Using this and other methods in his immunological work, he developed, together with N. A. Mitchison and N. K. Jerne, the antigen-bridge model of T-B cell cooperation, identified germinal centers as the sites of antibody somatic hypermutation, the B cell antigen receptor as a survival determinant of B cells, and the germinal center as a major site of human B cell lymphomagenesis, including Hodgkin lymphoma. Over the last years the work of his group has focused on mechanisms of microRNA control and the development of mouse models of human B cell lymphomas.

After postdoctoral work at the Institut Pasteur in Paris he built an immunology department at the Institute for Genetics at the University of Cologne, where he stayed for 38 years, was the founding Program Coordinator of the EMBL Mouse Biology Program at Monterotondo near Rome, worked for 10 years at Harvard Medical School in Boston, and is since 2012 at the Max-Delbrück-Center for Molecular Medicine in Berlin, Germany.

Klaus Rajewsky won numerous scientific awards and is a member of several learned societies including the National Academy of Sciences of the USA and the American Academy of Arts and Sciences.

K. VijayRaghavan

Former Director of NCBS and InStem

K. (Vijay) Vijay Raghavan’s research aims to understand motor- and olfactory-circuit assembly: from deciphering how each component is made, interacts, and stabilizes to functioning in the animal to allowing behavior for in the real world. Related to the development of network function in the maintenance in the mature animal; another aspect of the work in the laboratory addresses how mature neurons and muscles are maintained. The laboratory uses a genetic approach, mainly using the fruit fly but also collaborating with those using mouse and cell-culture.

VijayRaghavan is Distinguished Professor of the National Centre for Biological Sciences (NCBS) of the Tata Institute of Fundamental Research (TIFR) in Bangalore, India and, since January 28, 2013, Secretary of the Department of Biotechnology Government of India. Before VijayRaghavan was the Director of NCBS and the interim head of InStem, a new institute being nurtured by NCBS. He continues to be active in research with his research laboratory at the NCBS in Bangalore.

He studied engineering at the Indian Institute of Technology, Kanpur. His doctoral work was at TIFR, Mumbai (Bombay University) and postdoctoral work at the California Institute of Technology.

VijayRaghavan was a member of the Science Advisory Council to the Prime Minister of India, Associate Member of the EMBO, Fellow of the Indian Academies of Sciences and a Fellow of the Royal Society. He is a JC Bose fellow of the Government of India