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Development and Evolutionary Morphogenesis - DEM

Ana Rita Cabral Martins Carlos


Cancer Senescence Disease tolerance Stress and damage responses Extracellular matrix Lama2 mutations

I did my PhD at the University of Oxford, in the UK, on the role of DNA damage responses in maintaining genomic stability and preventing tumorigenesis. During this period, I focused on understanding which DNA repair pathways and associated proteins are required for the repair of uncapped telomeres. I have also studied the senescence mechanisms associated with BRCA2 mutations.

Upon completion of my PhD in 2013, I moved back to Portugal, where I did my postdoctoral research at Instituto Gulbenkian Ciência. There I studied the importance of disease tolerance mechanisms, in particular iron-responsive mechanisms and metabolic adaptation, in the context of infection.

Now as an Assistant Researcher at the Development and Evolutionary Morphogenesis (DEM) group at the cE3c, Faculdade de Ciencias Universidade de Lisboa, I am studying the importance of preserving extracellular matrix (ECM) integrity in order to avoid cellular senescence and death mechanisms and to maintain disease tolerance.

My lines of research focus on:

  • How senescence or other p53-dependent mechanisms contribute to the onset of merosin-deficient congenital muscular dystrophy (MDC1A), a severe neuromuscular disease caused by mutations in LAMA2, which codes for a laminin that is a component of ECM.
  • How ECM contributes to maintain disease tolerance, i.e., a set of tissue damage control mechanisms that aim at safeguarding the organism, thus limiting the development of overt disease. This line of research allows to explore the importance of ECM in maintaining disease tolerance to different diseases including cancer.



ERRO 401

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