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Dr. rer. nat. Nieves Peltzer
Dr. rer. nat. Nieves Peltzer

Department of Translational Genomics

CMMC - Center for Molecular Medicine Cologne

University of Cologne

Robert-Koch-Straße 21

50931 Cologne

 

University of Cologne

Weyertal 115b

50931 Cologne

CV

Scientific degrees

2007 - 2012 PhD in Life Science, University of Lausanne, Switzerland
2005 - 2007 Master thesis (Research traineeship), La Plata University, Argentina and Institut Nationale de la Recherche Agronomique (INRA), Toulouse, France
2000 - 2006 Degree in Biotechnology, Quilmes University, Buenos Aires, Argentina

 

Scientific career

2012 - present Post-doctoral fellow at UCL Cancer Institute, London, UK
2007 - 2012 PhD student at the Physiology Department, University of Lausanne, Switzerland
02/2007 - 08/2007 Internship at Institut Nationale de la Recherch Agronomique (INRA), Toulouse, France
2005 - 2007 Intern and master student at Biochemistry and Molecular Biology Institute La Plata University, Buenos Aires, Argentina

 

Service to the scientific community and honours

2015 - 2016 Advanced Mobility Postdoc Fellowship awarded by the Swiss National Science Foundation (P300P3_158509)
2013 - 2015 Early Mobility Postdoc Fellowship awarded by the Swiss National Science Foundation (P2LAP3_148447)
02/2007 - 08/2007 ECOS-Sud fellowship. Financing Franco-Argentine internships

Publications

  • Cleavage of cFLIP restrains cell death during viral infection and tissue injury and favors tissue repair

    Cell death coordinates repair programs following pathogen attack and tissue injury. However, aberrant cell death can interfere with such programs and cause organ failure. Cellular FLICE-like inhibitory protein (cFLIP) is a crucial regulator of cell death and a substrate of Caspase-8. However, the…

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  • cIAPs control RIPK1 kinase activity-dependent and -independent cell death and tissue inflammation

    Cellular inhibitor of apoptosis proteins (cIAPs) are RING-containing E3 ubiquitin ligases that ubiquitylate receptor-interacting protein kinase 1 (RIPK1) to regulate TNF signalling. Here, we established mice simultaneously expressing enzymatically inactive cIAP1/2 variants, bearing mutations in the…

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  • Linear ubiquitin as a common regulator of cellular stress

    Linear or M1-ubiquitination (Ub) is required for optimal NF-kB activation and for cell death inhibition. Using Drosophila as a model organism, Aalto et al. found that hypoxia, oxidative and mechanical stress induced M1-Ub by the HOIP homolog, LUBEL. Increased M1-Ub had a protective function driven…

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  • Cell Death-Related Ubiquitin Modifications in Inflammatory Syndromes: From Mice to Men

    Aberrant cell death can cause inflammation and inflammation-related diseases. While the link between cell death and inflammation has been widely established in mouse models, evidence supporting a role for cell death in the onset of inflammatory and autoimmune diseases in patients is still missing.…

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  • RIPK1 and Caspase-8 Ensure Chromosome Stability Independently of Their Role in Cell Death and Inflammation

    Receptor-interacting protein kinase (RIPK) 1 functions as a key mediator of tissue homeostasis via formation of Caspase-8 activating ripoptosome complexes, positively and negatively regulating apoptosis, necroptosis, and inflammation. Here, we report an unanticipated cell-death- and…

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  • Cell Death and Inflammation - A Vital but Dangerous Liaison

    The immune system has developed multiple ways to fight infection. Yet, it is constantly tasked with overcoming newly developing pathogenic mechanisms of resistance to host immunity. In most mammals, the stimulation of both innate and adaptive immune receptors can result in gene activation and cell…

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