The Core Group (CG) constitutes the technical nucleus of the Action and it is in charge of the strategic direction. The CG constitutes also the Translational Think Tank, which mission is to identify clinically and biotechnology relevant projects to convert into medically relevant and/or industry valuable applications.

Arkaitz Carracedo Perez

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CIC bioGUNE
http://personal.cicbiogune.es
Spain
WG6
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Cancer metabolism and signaling, prostate cancer, breast cancer, preclinical trials, clinical studies, translational research
Carina Holmberg

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University of Helsinki
http://research.med.helsinki.fi
Finland
WG2
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Our work is focusing on identifying and characterizing molecular mechanisms and signaling pathways involved in regulation of proteasome function during an animal?s life. Specifically, we are interested in unraveling tissue-specific regulatory mechanisms and changes occurring during aging. By developing C. elegans models for real-time proteasome studies, we have obtained mechanistic insights into proteasome regulation and links between lifespan-regulating signaling pathways and the proteasome as well as found conserved regulatory functions on degradation of proteotoxic proteins in human cells. Translational research has been initiated to relate our findings to human age-associated disorders.
Christine Blattner

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Karlsruher Institut für Technologie (KIT). ITG-Institute of Toxicology and Genetics
http://www.itg.kit.edu
Germany
WG1
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We are interested in the regulation and function of p53, one of the most well-known tumor suppressor proteins. P53 plays an integral part in the DNA damage response and there is more and more evidence, that this protein is also important for the stemcell-phenotype and for differentiation of stem cells. In this cell type, we aim to clarify the precise role and regulation of p53. Another aspect in which we are interested is DNA repair in stem cells and in the question why the DNA damage response is so much more efficient in this cell type.
Dimitris Xirodimas

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CRBM (Macromolecular Biochemistry Research Centre). CNRS. UMR 5237
http://www.crbm.cnrs.fr
France
WG5
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Our research is focused on the ubiquitin-like molecule NEDD8. Our aim is to identify and characterise novel substrates for NEDD8 and understand how NEDDylation is controlled in cells. In particular we are exploiting our discoveries on the role of NEDD8 as sensor of cellular stress. Our initial studies demonstrated that in response to perturbations in cell growth the NEDD8 pathway causes the activation of the p53 tumour suppressor through the nucleolus. More recent studies identified a more general role for NEDD8 in cellular stress. In response to a variety of stress signals, including inhibition of 26S proteasome activity, heat shock, oxidative stress NEDD8 conjugation rapidly increases. However, this stress-induced NEDD8 conjugation is mediated through enzymes of the ubiquitin rather than of the NEDD8 pathway. By developing methods to specifically distinguish between NEDDylation and ubiquitination sites we found the formation of either poly-NEDD8 or mixed NEDD8-ubiquitin chains under stress. A key goal of our research is to elucidate the biological significance for the NEDD8 response upon stress conditions. We are using biochemical, biological, proteomic and currently developing genetic approaches (C.elegans) to address the above biological questions.
Efthimios M. C. Skoulakis

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Alexander Fleming Biomedical Sciences Research Centre
http://www.fleming.gr
Greece
WG6
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Neuroscience of Learning and memory, Fly models of learning and memory disabilities and neurodegenerative diseases. Olfaction and olfactory receptors
Elah Pick

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University of Haifa
http://sci2.haifa.ac.il
Israel
WG2
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Activation and activity of the COP9 signalosome; CRLs activity; developing CSN readout assay; NEDDylation/deneddylation; moonlighting within components of PCI complexes; The COP9 SIGNALOSOME in stress, cancer and neurodegeneration. The CSN/NEDD8 axis upon oxidative stress. Regulation of the Mevalonate pathway, also known as the Isoprenoid pathway by the COP9 signalosome.
Gemma Marfany

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Universitat de Barcelona. UB
http://www.ub.edu
Spain
WG6
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We are geneticists besides being molecular biologists. We actively search for genes involved in human hereditary visual diseases causing blindness. Another of our research lines is the characterization of the expression and function of deubiquitinating and SUMO-metabolism enzymes in the retina.
Henrique Girao

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IBILI-Institute of Biomedical Imaging and Life Sciences
http://www.uc.pt
Portugal
WG3
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We have been interested on the molecular mechanisms involved in the maintenance of quality control, with particular focus on non-canonical functions of ubiquitin on lysosomal degradation. For this purpose, we have been studying two main substrates, the HIF1-a, on the context of hypoxia-induced neovascularization, and CxIn our lab routine we use mammalian cell and organ cultures, biochemical techniques, protein manipulation (including overexpression and silencing), confocal and transmission electron microscopy43, involved in gap junction intercellular communication, on the context of heart diseases. In more detail, we have been using these proteins to evaluate the putative crosstalk between proteasome and autophagy, and autophagy and endocytosis
Isabelle Jupin

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Virologie Moleculaire. Institut Jacques Monod. UMR 7592 CNRS - Universite Paris 7
http://www.ijm.fr
France
WG1
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Our main research interest concerns the molecular mechanisms of viral RNA replication. Lately, we have obtained data regarding the importance of ubi- or deubiquitination processes in the control of viral multiplication. We have characterized a viral deubiquitinase (DUB) with very original properties in terms of substrate specificities and protein structure. We are currently studying its structure/function relationship, as well as its effects on cellular protein substrates.
Manuel Rodríguez

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CNRS - ITAV USR3505
http://www.cnrs.fr
France
WG1
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Our group has recently developed molecular traps to capture endogenous proteins modified by members of the ubiquitin family. The prototype traps named TUBEs (for Tandem Ubiquitin Binding Entities) capture ubiquitylated proteins from cells, tissues and organs. When associated to mass spectrometry, total ubiquitylated proteins can be captured after a treatment or during a physiological or pathological process. A pattern of ubiquitylation can be associated to particular responses providing biomarkers and potential drug targets.
Marc Piechaczyk

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Institut de Génétique Moléculaire de Montpellier. CNRS
http://www.igmm.cnrs.fr
France
WG6
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We are aiming at both better understanding the mechanisms of oncogenesis and improving anticancer treatments. Most pertinent in the frame of this COST application, we are studying (i) how ubiquitylation/sumoylation/degration of the ubiquitous AP-1 transcription complex contribute to tumorigenesis and (ii) how the ROS/SUMO axis contribute to resistance of certain leukemia to chemotherapy. In the latter case, our work partly rely on a mouse model that also permit to improve monoclonal antibody-based anticancer treatments, leading us to investigate AP-1 and sumoylation in immune cells.
Michael Glickman

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Technion
No website
Israel
WG2
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Current research topics 1) Proteasome structure and function, 2) Proteomic charting the cellular ubiquitin-linkage profile 3) Reciprocal relationship between ubiquitination-dependent-degradation and mitochondria function and dynamics. 4) Recognition of ubiquitin and ubiquitin-like signals
Michael John Clague

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University of Liverpool
http://pcwww.liv.ac.uk
United Kingdom
WG3
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Endocytosis, RTK trafficking and signaling. Deubiquitylation in pathways germane to cancer
Nico Dantuma

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Karolinska Institutet
http://twitter.com
Sweden
WG1
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Developing reporter assays for ubiquitin-dependent proteolysis Understanding basic principles of the ubiquitin/proteasome system The ubiquitin/proteasome system in neurodegenerative disorders Ubiquitin signaling in the DNA damage response
Olivier Coux

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CRBM (Macromolecular Biochemistry Research Centre). CNRS. UMR 5238
http://www.crbm.cnrs.fr
France
WG2
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Cell biology and biochemical approaches to dissect many aspects of the specificity and mechanism of action of the ubiquitin-proteasome system, in the context of cell cycle
Pascale Bomont

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INM-INSERM U151. Hospital St Eloi
http://www.inmfrance.com
France
WG2
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Our research program aims to address the direct role of the Ubiquitin Proteasome System (UPS) in neurodegeneration. For that purpose, we focus on Giant Axonal Neuropathy (GAN), a fatale neurodegenerative disorder caused by recessive mutations in gigaxonin, the substrate adaptor of a Cul3-
Petek Ballar

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Ege University
http://www.ege.edu.tr
Turkey
WG4
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Ubiquitin mediated proteasomal degradation, Endoplasmic Reticulum associated degradation
Rosa Barrio

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CIC bioGUNE
http://personal.cicbiogune.es
Spain
WG3
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We investigate biomedically relevant genes and processes using Drosophila melanogaster and mouse as model systems, as well as human cells. We are interested on the role of SUMOylation in development, steroidogenesis, ciliogenesis and growth, through the modification of transcription factors.
Rosa Farràs Rivera

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Centro de Investigación Principe Felipe CIPF
http://www.cipf.es
Spain
WG6
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A major focus of our work is to understand the regulatory mechanisms of protein turnover of cell cycle-related proteins and how these processes impact on proliferation, differentiation and tumorigenesis. This is a critical area of cancer research, since accelerated cell growth and deregulated protein turnover is a major feature of tumour formation and progression. In addition, cellular differentiation is also associated with the regulation of protein turnover and often antagonises carcinogenesis. We believe that a better understanding of the molecular basis of malignant transformation will lead not only to further advances in cancer biology but also to help develop novel and effective cancer therapies.
Sebastien Leon

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Institut Jacques Monod - CNRS - Université Paris Diderot
http://tinyurl.com
France
WG1
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Our team focuses on the regulation of membrane protein trafficking by ubiquitin, using the yeast Saccharomyces cerevisiae as a model system. We are particularly interested in understanding the molecular mechanisms governing plasma membrane proteome remodeling in the face of nutritional challenges (Becuwe et al., J Cell Biol 2012 ; Becuwe & Leon, eLife 2014). The key goals are to elucidate the mechanisms in charge of the nutrient-regulated ubiquitylation of transporters, and how this regulates their localization. Our approaches range from cell biology techniques (live cell microscopy, microfluidics, BiFC), genetics and biochemistry (in vivo and in vitro ubiquitylation, interaction proteomics) to systems-wide approaches (genetic screens, high-throughput imaging).
Wiep Scheper

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VU University Medical Center
http://www.cncr.nl
Netherlands
WG4
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Molecular analysis of the role of proteostasis in Alzheimer?s disease pathogenesis, using cell and animal models as well as human post-mortem brain material