Professor Seamus Martin

Seamus Martin holds the Smurfit Chair of Genetics at Trinity College Dublin, Ireland (since 1999). He was elected to The Royal Irish Academy in 2006, to the European Molecular Biology Organization (EMBO) in 2009 and to Academia Europaea in 2023. He served as President of the European Cell Death Organization (ECDO) from 2016-2018 and was awarded an ERC Advanced grant in 2021. He co-wrote (with Pete Delves, Dennis Burton and Ivan Roitt) the 11th, 12th and 13th Editions of the classic undergraduate Immunology textbook `Essential Immunology" and has served as Editor-in-Chief of The FEBS Journal (Cambridge, UK), an international life sciences journal, since 2014 to present. The Martin laboratory is interested in all aspects of programmed cell death, especially the links between cell death, inflammation and cancer. Some key papers: Introduction of annexin V-labelling, the gold standard for measuring apoptosis (Martin et al., 1995 J. Exp. Med.), Unravelling the apoptosis-associated caspase activation cascade (Slee et al., 1999 J. Cell Biol.), Oncogenic Ras promotes autophagic cell death (Elgendy et al., 2011 Molecular Cell), Apoptotic cells can be pro-inflammatory (Cullen et al., 2013 Molecular Cell; Henry et al., 2017 Molecular Cell), Parkin activation can promote apoptosis (Hollville et al., 2014 Molecular Cell; Carroll et al., 2014 Cell Reports) Discovery of the mechanism of activation of the IL-36 cytokine family (Henry et al., 2016 Cell Reports; Clancy et al., 2018 Cell Reports); ER Stress promotes inflammation via TRAIL receptors (Sullivan et al., 2020 Developmental Cell); IL-37 is pro-inflammatory via IL-36 receptor engagement (Sullivan et al., 2022 Science Immunology). Necrotic cell death either instigates inflammation (in sterile injury contexts) or is a key amplifier of inflammation (during infection). In both scenarios, molecules released from dead cells (collectively called DAMPs, damage-associated molecular patterns) trigger inflammation. However, exactly what constitutes a DAMP has been the subject of much debate. We are currently exploring the idea that members of the extended IL-1 family constitute the key DAMPs and how IL-1 family cytokines become activated/inactivated. We are also actively exploring how cell stress (e.g. due to chemotherapy) triggers inflammation. Editor-in-Chief of The FEBS Journal (since Jan 2014-present) Current and previous Editorial Board memberships: Cell Reports (Cell press), Science Signaling (AAAS), Oncogene (Deputy editor & Receiving Editor), The Journal of Biological Chemistry, Cell Death and Differentiation (Nature Publishing Group), Oncogenesis (Nature Publishing Group). "FEBS Open Bio (FEBS Press). National and international awards: Wellcome Trust Prize Fellowship Award (1994-1996) Wellcome Trust Senior Fellow Award (1996-2001) Science Foundation Ireland Awards (2002-07, 2008-14, 2015-20) The BA Charles Darwin Award (2005) The GlaxoSmithKline Award of The Biochemical Society UK (2006) Elected to The Royal Irish Academy (2006) Elected to the European Molecular Biology Organization (EMBO) in 2009 The Boyle Medal (2015), Ireland"s highest scientific honor, awarded every 4 years. The ICDS Medal (2016), The major biannual award from the International Cell Death Society. European Research Council (ERC) Advanced Grant Awardee 2021-present Elected to Academia Europaea, 2023

  Antisera   Apoptosis   Apoptosis, molecular control   Autophagy   Biochemical Markers   Biological Markers   Biological Response Modifiers   Biology   Biomedical sciences   Caenorhabditis elegans   Cancer Biology   Cancer chemotherapeutic drugs- mode of action   Cancer chemotherapy   Cancer genetics and cell biology including metastasis   Cancer/Carcinogenesis   Caspase proteases   Cell and tissue maintenance, repair and ageing   Cell Communication   Cell Components   Cell cycle control   Cell Death   Cell Lines   Cellular, molecular and developmental immunology   Chemotherapeutic Agents   Chemotherapy   Chronic inflamation   Commercialisation of scientific research   Cytotoxic T cell Killing   DIABLO   Genetics   Genomic structure and function, molecular approaches to gene function   Granzymes   HIV virology and pathogenesis   Immune Enhancers   Immune system   Immune System Disorders   Immunity   Immunization   Immunogenetics   Immunology   Immunopathology   Immunotherapies for Cancer   Immunotherapy   In Vitro Testing, Trial Methods   Inflammation   INHIBITION   Innate immunology   Intra and intercellular signalling   Leukemia   Leukemias and lymphomas   Leukocyte Biology   Lymphocytes   Lymphoma   Medical Sciences, Research   Mitochondrial fission & fusion mechanisms   Molecular Biology   Molecular Cloning   Molecular Genetics   Molecular/Cellular Entities   Monoclonal Antibodies   OLIGOMERIZATION   Oncogenes, apoptosis and tumour development   Programmed Cell Death   PROTEIN   Proteins and Macromolecules   Proteomics   Screening of Drugs/Agents   SMAC   Tissue Culture   Toxicity and toxinology   Tumour immunology and immunotherapy   Vaccine   Virology and viral pathogenesis

The Martin laboratory is interested in all aspects of programmed cell death, especially the links between cell death, inflammation and cancer. Some key papers: Introduction of annexin V-labelling, the gold standard for measuring apoptosis (Martin et al., 1995 J. Exp. Med.), Unravelling the apoptosis-associated caspase activation cascade (Slee et al., 1999 J. Cell Biol.), Oncogenic Ras promotes autophagic cell death (Elgendy et al., 2011 Molecular Cell), Apoptotic cells can be pro-inflammatory (Cullen et al., 2013 Molecular Cell; Henry et al., 2017 Molecular Cell), Parkin activation can promote apoptosis (Hollville et al., 2014 Molecular Cell; Carroll et al., 2014 Cell Reports) Discovery of the mechanism of activation of the IL-36 cytokine family (Henry et al., 2016 Cell Reports; Clancy et al., 2018 Cell Reports); ER Stress promotes inflammation via TRAIL receptors (Sullivan et al., 2020 Developmental Cell); IL-37 is pro-inflammatory via IL-36 receptor engagement (Sullivan et al., 2022 Science Immunology). Necrotic cell death either instigates inflammation (in sterile injury contexts) or is a key amplifier of inflammation (during infection). In both scenarios, molecules released from dead cells (collectively called DAMPs, damage-associated molecular patterns) trigger inflammation. However, exactly what constitutes a DAMP has been the subject of much debate. We are currently exploring the idea that members of the extended IL-1 family constitute the key DAMPs and how IL-1 family cytokines become activated/inactivated. We are also actively exploring how cell stress (e.g. due to chemotherapy) triggers inflammation Molecular Control of Apoptosis (programmed cell death). Natural Killer Cell and CTL proteases (particularly granzyme B) and their mode of action. The role of Bcl-2 family proteins in chemoresistance in cancer. The role of caspases in inflammation. IL-1 family cytokines and inflammation. Cell Stress and Inflammation. Cell Senescence and Inflammation. Cancer chemotherapy. Regulation of entry to cell senescence by chemotherapy.