Action Members are any researcher who participates actively in PROTEOSTASIS. All Members belong to one or more Working Group. Members can include researchers from COST Countries, Near Neighbour and International Partner Countries.
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Bernat Crosas Navarro Please log-in to see email and phone. |
Instituto de Biología Molecular de Barcelona http://www.ibmb.csic.es Spain |
WG2 |
| To examine novel levels of regulation of the proteasome pathway focusing on the mechanisms that control proteasome function and its interaction with protein substrates | |||
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Bertrand Friguet Please log-in to see email and phone. |
University Pierre and Marie Curie (UPMC) http://www.ibps.upmc.fr France |
WG6 |
| Our goals are to elucidate the role of protein oxidation as well as oxidized protein degradation and repair during cellular ageing in vitro and ex vivo and in situations of oxidative stress leading to accelerated ageing. We are also currently investigating the relationship between oxidative stress, protein homeostasis and circadian rhythmicity in relevant cellular models. | |||
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Boris Turk Please log-in to see email and phone. |
Department of Biochemistry and Molecular Biology. J. Stefan Institute http://www-b1.ijs.si Slovenia |
WG6 |
| Speciality: Inflammation-associated diseases and the role of proteolysis in their onset and progression. We are primarily focusing on lysosomal cysteine cathepsins and understanding their role in these diseases, largely cancer and arthritis. We are combining different approaches, including identification of physiological substrates and developing/characterizing activity-based probes for in vivo monitoring of enzyme activities, which includes both intra and extracellular proteolysis. Skills: Biochemistry of proteases including assay development, proteomics, in vivo imaging in mice, molecular and cell biology Facilities: Proteomics facility, IVIS Spectrum in vivo imaging system, Leica confocal microscope, small animal facility, X-ray crystallography, protein expression and purification facilities, ? MRI facility for small animals available at the Institute | |||
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Brenda A. Schulman Please log-in to see email and phone. |
Max Planck Institute of Biochemistry http://www.biochem.mpg.de Germany |
WG2 |
| Mechanisms and regulation of ubiquitin and ubiquitin-like protein conjugation. | |||
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Bruno Andre Please log-in to see email and phone. |
Université Libre de Bruxelles http://www.mpc-ulb.be Belgium |
WG3 |
| Molecular yeast genecics - Role of Ub in signaling and control of membrane trafficking | |||
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Carina Holmberg Please log-in to see email and phone. |
University of Helsinki http://research.med.helsinki.fi Finland |
WG2 |
| 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. | |||
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Carmela Giglione Please log-in to see email and phone. |
Institute for Integrative Biology of the Cell (I2BC) http://www.i2bc.paris-saclay.fr France |
WG1 |
| The group investigates basic mechanisms, roles and impact on protein fate of these NPM in both prokaryotes and eukaryotes. To investigate these modifications and the enzymes involved, the group has put major efforts in developing an integrative strategy, involving reverse and chemical genomics, structural-proteomics approaches, setting new bio-informatics tools as well as cell biology analysis. Particularly, our needs in new proteomics and structural tools pushed us to i) become the support staff of the MS platform at I2BC ii) exploit both Soleil and ESRF Synchrotrons and iii) attract brilliant technical specialized researchers. We use mainly Arabidopsis thaliana as a model system because of its convenience relative to our research topic but others models are currently used (e.g., bacteria, archaea and cyanobacteria, plant and mammal cell cultures, yeast). Indeed, since the enzymes involved in NPM are conserved, we translate and confirm the results obtained in Arabidopsis in other prokaryotic and eukaryotic organisms. The team also displays a side activity on therapeutic applications. Since the enzymes of NME and MYR are considered excellent targets to combat various diseases, we take advantage of our knowledge to develop new inhibitors which could be used as pharmacological probes to investigate various pathologies or as new leads for potential therapeutic use. | |||
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Carmen Doina Manciuc Please log-in to see email and phone. |
St. Parascheva Infectious Diseases Clinical Hospital. Iasi. Romania http://www.gomi.ro Romania |
WG6 |
| Speciality: Infectious diseases patients; HIV/AIDS patientsSkills: - clinical skills- lumbar punction technique | |||
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Carmen Rivas Please log-in to see email and phone. |
Centro Nacional de Biotecnología. CSIC http://www.cnb.csic.es Spain |
WG6 |
| Our group is interested in the relationship between virus and cancer. Tumor-viruses induce oncogenesis through manipulating an array of different cellular pathways, some of which are extensively regulated by the small ubiquitin-like protein SUMO. SUMOylation is a reversible posttranslational modification, in which SUMO is covalently attached to a target protein and changes its activity, subcellular localization and/or interaction with other macromolecules. Modification by SUMO is involved in many biological functions, and there are some evidences that implicate misregulated SUMOylation in tumorigenesis. The relevance of SUMO conjugation in virus replication is illustrated by the discovering that many host proteins involved in innate and intrinsic immunity are regulated by SUMOylation, and that SUMO is a contributor to the regulatory process that governs the initiation of the type I interferon (IFN) response. Furthermore, the importance of SUMO is exemplified by the fact that viruses have evolved means to take advantage of the conserved host cell SUMOylation machinery, by either modulating essential components or being targets of this post translational modification themselves. Based on these data we are now interested in (i) identifying how viruses and their regulatory proteins exploit the host cell SUMO modification system; (ii) evaluating the role of SUMO modification in virus replication, and (iii) determining how an alteration in the SUMOylation pathways by tumor viruses may have an impact on cell transformation. | |||
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Caroline Jefferies Please log-in to see email and phone. |
Molecular and Cellular Therapeutics. Royal College of Surgeons in Ireland http://research1.rcsi.ie Ireland |
WG3 |
| Systemic lupus erythematosus (SLE) is a chronic, multisystem autoimmune disease that affects about 0.1% of our population, predominantly women. It has been over 40 years since a new drug has been approved for specific use in the treatment of SLE. There is therefore an unmet need for new targeted therapies. Recent work has linked high levels of the type I interferons observed in SLE patients with both the pathology and the severity of the disease. Our focus has been to identify novel negative regulators of TLR-induced interferon production, with the aim of developing strategies to manipulate their activity for the treatment of SLE. | |||
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Catarina R. Almeida Please log-in to see email and phone. |
University of Aveiro http://www.ua.pt Portugal |
WG2 |
| Earlier in my career I did a PhD in Immunology, particularly on what regulates the function of Natural Killer (NK) cells when interacting with target cells. I then worked in Regenerative Medicine, and studied the impact of immune responses on stem cell behavior. Overall, I have been learning how cell communication contributes to maintain tissue Homeostasis. More recently, I have become interested in understanding how to regulate proteostasis in the elder, using as a model, immune cells. | |||
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Catherine Lindon Please log-in to see email and phone. |
University of Cambridge http://www.gen.cam.ac.uk United Kingdom |
WG5 |
| Ubiquitin-mediated proteolysis during cell division, with particular interest in molecular mechanisms regulating stability of Aurora kinases. | |||
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Chris Bowler Please log-in to see email and phone. |
Institut de Biologie de l'Ecole Normale Supérieure (IBENS). CNRS http://www.biologie.ens.fr France |
WG3 |
| Arabidopsis and marine diatoms as experimental systems for exploring cellular functions in response to environmental signals.ChIP and ChIP-seq, RNA-seq, genome and epigenome sequencing and related bioinformatics, molecular genetics, biochemistry, ecological analysis of community structure. | |||
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Christa Jane Maynard Please log-in to see email and phone. |
Karolinska Institutet http://ki.se Sweeden |
WG3 |
| Speciality: Autophagy in neurodegenerative disease and aging.Skills: Cell and molecular biology techniques (eg. generating expression constructs for expression of aggregation-prone proteins and reporters in mammalian cell lines). Confocal, fluorescence and light microscopy; transgenic mouse techniques (cross-breeding, analysis of tissues with histological and protein chemistry methods). Protein chemistry techniques, eg. Western blotting, IP. | |||
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Christel Brou Please log-in to see email and phone. |
Institut Pasteur http://www.pasteur.fr France |
WG1 |
| We study the Notch pathway, which is involved in the development and maintenance of organs and tissues. Contrary to a number of signaling pathways, Notch does not use a cascade of kinases, but relies on complex trafficking events targeting both the receptor and its ligands, and controlled by a network of ubiquitinated proteins and ubiquitin receptors. We specifically study the mechanisms that control the maintenance of an active receptor at the plasma membrane, the production of active ligands, and the regulation of signal transduction after activation. We are particularly interested in the trafficking and post-translational modifications undergone by the Notch receptor and its ligands. | |||
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Christian Behl Please log-in to see email and phone. |
Institute for Pathobiochemistry. University Medical Center of the Johannes Gutenberg University Mainz http://www.unimedizin-mainz.de Germany |
WG2 |
| Investigation of the cellular and molecular mechanisms of neurodegeneration with a particular focus on age-associated biochemical alterations in vitro and in vivo. AD, PD, ALS and stroke models are used. Prominent research topics are (1) protein quality control and (2) protein degradation systems (proteasome, autophagy). Here, protein quality control, aggregation and degradation in the context of ageing and disease are studied. In particular, we are working on the characterization and regulation of selective macroautophagy, for instance the identification of new physiological and pharmacological autophagy modulators. | |||
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Christian Gaiddon Please log-in to see email and phone. |
INSERM-Strasbourg University http://gaiddon-lab.com France |
WG2 |
| 1) Analysis of expression of specific genes including miRNA coding genes (RT-qPCR, Western blot); 2) perform gain and loss of function studies (siRNA, mimick, antimir, exp. vectors); 3) Biochemical survival assay and cell death; 4) immune-cytochemistry and histochemistry; 4) in vivo evaluation of anticancer activity (xenografts); 5) in vivo evaluation of muscle atrophy; 6) primary culture of neurons; 7) Transgenic models development; 8) Analysis of patients biopsies; 9) physicochemical characterization of organometallic compounds | |||
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Christian Widmann Please log-in to see email and phone. |
Department of Physiology. Faculty of Biology and Medicine. University of Lausanne. Switzerland http://www.unil.ch Switzerland |
WG2 |
| Speciality:Three main topics are investigated in the laboratory, the first two being most directly relevant to the present COST action. Topic 1. The caspase-3/RasGAP stress sensor module and the control of cell metabolism. We study a cellular device that senses the activity of the caspase-3 protease. This module is composed of caspase-3 itself and one of its substrates called RasGAP. Depending on the extent of RasGAP cleavage, cell activates survival or pro-death responses. The non-lethal functions of this module involve regulations of transcription factors and modulation of cell metabolism. Topic 2. Anti-tumor activity of RasGAP-derived peptides. One of the smaller fragments generated by caspase-3-mediated cleavage of RasGAP, called fragment N2 (corresponding to the 158-455 sequence of RasGAP), is able to sensitize tumor cells, but not normal cells, to genotoxin-induced death. The sensitizing activity of fragment N2 resides in a 10 amino acid sequence at position 317-326, which is located within the SH3 domain of RasGAP. When chemically sensitized and hooked to a cell-permeable peptide derived from the HIV TAT protein, the resulting compound, called TAT-RasGAP317-326, efficiently sensitizes tumor cells, but not normal cells, to genotoxin- and photodynamic therapy-induced death. We are currently trying, one the one hand, to determine the mode of action of the peptide, and on the other hand, to identify small molecules that mimic the anti-cancer properties of the RasGAP-derived peptide. Topic 3. Unraveling the mechanisms of HDL-mediated pancreatic beta cell protection. High-density lipoproteins (HDLs) exert potent protective functions on pancreatic beta cells. How this operates at the molecular level is not known. The goal of the project is to identify the HDL components, their cellular receptors, and the signaling pathways they activate that mediate the protective effects of HDLs on pancreatic beta cells. Skills: Cell death assessment, cell metabolism assessment, somatic knock-out, in vivo mouse models, lentivirus usage. | |||
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Christiane Funk Please log-in to see email and phone. |
Umeå University:Dept of Chemistry and Umeå Plant Science Centre http://www.upsc.se Sweden |
WG4 |
| Biochemistry, proteomics, molecular biology | |||
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Christine Blattner Please log-in to see email and phone. |
Karlsruher Institut für Technologie (KIT). ITG-Institute of Toxicology and Genetics http://www.itg.kit.edu Germany |
WG1 |
| 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. | |||
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Christos DELIDAKIS Please log-in to see email and phone. |
Foundation for Research & Technology. Hellas/ Institute of Molecular Biology & Biotechnology http://www.imbb.forth.gr Greece |
WG3 |
| Speciality: (a) Developmental genetics of bHLH-O proteins with emphasis on neural development. (b) Elucidating the mechanism of DSL-Notch signalling, especially the role of ligand ubiquitylation and endocytosis. Skills: Drosophila genetics. Cell culture. (Immuno)fluorescence and confocal microscopy of cells and tissues. Protein biochemistry. Protein ubiquitylation. Gene expression and reporter genes. | |||
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Ciaran Gerard MORRISON Please log-in to see email and phone. |
No website Ireland |
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Cláudia Santos Please log-in to see email and phone. |
Institute of Experimental Biology and Technology (iBET) http://www.itqb.unl.pt Portugal |
WG6 |
| Polyphenols bioaccessability and bioavailability (in vitro digestion, human intervention studies and brain permeability). In particular study of the molecular mechanisms affected by plant phenolic compounds on inflammation, cancer, hematological and neurodegenerative diseases by using humanized yeast and mammalian cell models (including neuroinflammation, neurodegenaration, blood brain barrier integrity and Parkinson disease cell models). | |||
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Claudio Joazeiro Please log-in to see email and phone. |
Universitaet Heidelberg (ZMBH) http://www.zmbh.uni-heidelberg.de Germany |
WG1 |
| Ubiquitin, protein quality control, ribosome-associated quality control, molecular mechanisms of neurodegeneration | |||
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Claus Schwechheimer Please log-in to see email and phone. |
Technische Universität München - Weihenstephan http://www.wzw.tum.de Germany |
WG3 |
| Plant signal transduction, NEDD8 modification, Arabidopsis, identification of novel NEDD8 modified proteins | |||
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Colin Adrain Please log-in to see email and phone. |
Instituto Gulbenkian de Ciência http://www.igc.gulbenkian.pt Portugal |
WG4 |
| My lab is interested in how membrane trafficking and membrane protein quality control mechanisms coordinate cellular signaling during normal physiology, and disease. 60% of all current drugs target membrane proteins, illustrating the medical importance of this pathway. However the complex biogenesis and trafficking of many signaling proteins is poorly understood, providing an incentive to understand the secretory pathway better. The endoplasmic reticulum (ER) is the portal to the secretory pathway, through which one third of the entire translated genome passes. It fulfills many important roles: protein biogenesis, protein quality control, ER-associated degradation (ERAD) of misfolded proteins, and regulation of the anterograde trafficking of secretory proteins to other destinations within the secretory pathway. Until recently, it was believed that secretory traffic was accomplished by a default mechanism called bulk flow whereby newly synthesized proteins are packaged into trafficking vesicles at the rate that they are produced. However, it is now clear that trafficking, especially of membrane proteins, is controlled by additional influences, including cargo receptors, trafficking partners, post-translational modifications or regulation of protein stability. We elaborate this theme of trafficking control over signaling in the projects indicated below, using a combination of mouse genetics, disease models, cell biology and biochemistry. The lab combines cellular biochemistry and mutant mouse models. | |||
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Corrado Santocanale Please log-in to see email and phone. |
National University of Ireland Galway http://www.chromosome.ie Ireland |
WG5 |
| Research focus on elucidating the molecular mechanisms of DNA replication in cancer cells and exploiting the results of this research for therapeutic purposes. Active projects focus on understanding the cellular functions and regulation of Cdc7 kinase and on characterizing inhibitors of Cdc7 kinase activity in breast cancer models. More recently we have been involved in understanding how deubiquitinylating enzymes contribute to the stability of replication fork and promote genome stability. | |||
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Cristina Muñoz Pinedo Please log-in to see email and phone. |
Bellvitge Biomedical Research Institute (IDIBELL) http://www.idibell.cat Spain |
WG2 |
| Methods to study cell death in vitro and cellular signaling due to starvation, including FACS, real-time microscopy and other techniques. Work with murine primary neurons and mouse models of cancer (xenografts). | |||
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Dan Lindholm Please log-in to see email and phone. |
Institute of Biomedicine. University of Helsinki http://www.biomed.helsinki.fi Finland |
WG3 |
| Neuronal diseases ER stress Mitochondria E3 ubiquitin ligases and DUBS | |||
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Daniel A. Chamovitz Please log-in to see email and phone. |
Tel Aviv University http://www.danielchamovitz.com Israel |
WG3 |
| The COP9 Signalosome in Drosophila and Arabidopsis | |||