Data-Gouv-ML/pcri-informations-sur-les-projets-laureats huggingface dataset:
Improved Cryopreservation using Ice Binding Proteins (CRYOPRESERVATION)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Applied life sciences and biotechnology
Countries involved: Israel
Call:  (ERC-2011-StG_20101109, 2011)
Start date: 2011-11-01
End date: 2016-10-31
Duration (months): 60.0
Total project cost (EUR): 1500000.0
EU funding (EUR): 1500000.0
Participants: 1
Project status: CLOSED

Several organisms have evolved specialized ice binding proteins (IBPs) that prevent their body fluids from freezing (antifreeze proteins, AFPs), inhibit recrystallization of ice in frozen tissues, or initiate freezing at moderate supercooling temperatures (ice nucleating proteins, INPs). These proteins have many potential applications in agriculture, food preservation, cryobiology, and biomedical science. The ubiquitous presence of IBPs in such organisms indicates the power of these molecules to enable survival under cold conditions. Despite this key role in nature, however, IBPs have been effectively exploited in only one cryopreservation application, namely, recrystallization inhibition in ice cream. Several terrestrial organisms, including insects, have developed very active forms of AFPs. These hyperactive AFPs (hypAFPs) have not been utilized significantly thus far in cryopreservation techniques. The gap between the obvious potential of IBPs and their actual applications stems from a lack of knowledge regarding the mechanisms by which IBPs interact with ice surfaces and how these proteins can assist in cryoprotection. I propose to investigate the mechanism by which IBPs inhibit ice crystallization and the use of such proteins for cryopreserving cells, tissues, and organisms. My group has a strong record in the study of the interactions between IBPs and ice using novel methods that we have developed, including fluorescence microscopy techniques combined with cooled microfluidic devices. We will investigate the interactions of AFPs with ice and the use of hypAFPs in cryopreservation procedures. This research will contribute to an understanding of the mechanisms by which IBPs act, and apply the acquired knowledge to cryopreservation. The successful implementation of IBPs in cryopreservation would revolutionize the field of cryobiology, with enormous implications for cryopreservation applications in general and the frozen and chilled food industry in particular.

Keywords: cryopreservation,antifreeze proteins (afp),thermal hysteresis,hyperactive afp,ice physics,superheating,recrystallization,vitrification,gfp,microfluidics,confocal microscopy
Topographic signaling and spatial landmarks of key polarized neuro-developmental processes (YODA)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Neurosciences and neural disorders
Countries involved: France
Call:  (ERC-2011-StG_20101109, 2011)
Start date: 2012-04-01
End date: 2017-03-31
Duration (months): 60.0
Total project cost (EUR): 1498971.0
EU funding (EUR): 1498971.0
Participants: 1
Project status: CLOSED

Polarization, which confers asymmetry at molecular, cellular and tissue scales, is a fascinating process establishing fundamental features of biological systems. In multicellular organisms, symmetry breaking triggers the specification of embryonic body axes, governing the positioning of subsequent morphogenetic processes. Cells and tissues acquire complex polarity features, which remarkably, are highly precisely positioned within the body axes. How are polarization processes spatially oriented remlains fully enigmatic. During the formation of the nervous system, some crucial processes are polarized. Likewise, the navigation of neuronal projections in the body is a typical polarized process, axons selecting specific pathways to reach their targets. Studies in this field established crucial roles for topographic cues in controlling the polarized growth of neuronal projections. Up to now, my lab has focused on axon guidance mechanisms and while investigating the links between spatial position and neural circuit formation, I became convinced that topographic signalling must be equally required to set other key polarized processes of the developing nervous system. For example in the neuroepithelium, progenitor division is polarized along the apico-basal axis of the neural tube. Likewise in the young post-mitotic neuron, precise coordinates along the body axes define the site where the axon emerges. First, we postulate the existence of a topographic signaling giving to neuronal cells (but this might be a more general case) landmarks of the different embryonic axes so that polarization takes place with appropriate spatial orientation. Second, we make the assumption that this topographic signalling is ensured by cues initially identified for their role during axon navigation. Our goals are to explore these issues, using as a model the sensorimotor circuits, where several processes can be investigated for questioning the interplay between polarity and topography.

Keywords: axon guidance cues,polarity,topography,neuroepithelium,progenitor,axon,neural tube
TargetIng novel MEchanisms of Resolution in inflammation (TIMER)

Framework: FP7 — Cooperation
Programme: Health
Destination: Biotechnology, generic tools and medical technologies for human health
Action type: Collaborative project
Countries involved: Brazil,Switzerland,United Kingdom,Ireland,Italy
Call:  (FP7-HEALTH-2011-single-stage, 2011)
Start date: 2012-01-01
End date: 2015-12-31
Duration (months): 48.0
Total project cost (EUR): 3989175.67
EU funding (EUR): 2999300.0
Participants: 13
Project status: CLOSED

Resolution of inflammation is a key determinant of pathology, and an active process which involves diverse pathways and molecules. The general objective of the TIMER Consortium is to identify and validate new molecules involved in the resolution of inflammation as a basis for the development of innovative therapeutic strategies in chronic inflammatory and autoimmune diseases. The project will involve discovery of new natural or synthetic “pro-resolving” molecules for plant and animals and investigation on endogenous inflammation “pro-resolving” mechanisms identified by various partners of the Consortium, including atypical chemokine receptors, decoy receptors, and microRNA. Tapping resources of natural compounds will be a major thrust. Efforts will be mainly focused on the regulation by “pro-resolving” agents on two molecular systems of key relevance in inflammation: the chemokine system, which regulates recruitment, permanence and egress of leukocyte in tissues; and the TLR/IL-1R system, which is central for the activation of infiltrating leukocytes. To this purpose, the project will capitalize on, and bring added value to a strong tradition of the Consortium in the fields of: leukocyte recruitment and activation; negative regulators of inflammation; industrial-academic collaboration; identification and characterization of innovative inhibitors of natural origin; European-Brazilian collaboration.

Keywords: resolution of inflammation,tlr,atypical receptors,chemokines,natural compounds
Intracellular antibody Immunity (IAI)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Immunity and infection
Countries involved: United Kingdom
Call:  (ERC-2011-StG_20101109, 2011)
Start date: 2012-01-01
End date: 2016-12-31
Duration (months): 60.0
Total project cost (EUR): 1124340.0
EU funding (EUR): 1124340.0
Participants: 1
Project status: CLOSED

Antibodies are a critical component of immune defence but they provide purely extracellular protection – once inside a cell, a pathogen is safe. This is the view of humoral immunity that has existed for over 100 years. However, recent work in my lab has led to the discovery of a missing system of antibody-mediated immunity that takes place inside infected cells. I have identified a novel cytosolic antibody receptor (TRIM21) that binds to antibody-coated viruses after cellular infection and targets them for degradation in the proteasome. Importantly, TRIM21-mediated immunity is capable of clearing a cell of virus within hours of infection. This discovery represents a paradigm shift in how we think about viral immunity and offers the potential for new types of antiviral drugs. This grant application outlines key experiments to determine how intracellular antibody immunity works, what it works against and how we can augment or replicate it in the treatment of disease.

Keywords: antibodies,virology,neutralization
NCDs and their social determinants in Mediterranean partner countries: building sustainable research capacity for effective policy intervention (RESCAP-MED)

Framework: FP7 — Cooperation
Programme: Health
Destination: Optimising the delivery of healthcare to European citizens
Action type: Coordination and support actions
Countries involved: United Kingdom,United Kingdom,Ireland,Türkiye,Palestine, State of,Jordan,Lebanon,Switzerland,Tunisia,Syrian Arab Republic
Call:  (FP7-HEALTH-2011-single-stage, 2011)
Start date: 2012-01-01
End date: 2014-12-31
Duration (months): 36.0
Total project cost (EUR): 2226435.0
EU funding (EUR): 1986255.0
Participants: 12
Project status: CLOSED

The main purpose of RESCAP-MED is to enhance the non-communicable diseases (NCDs) research landscape in southern and eastern Mediterranean countries by (a) strengthening capacity in a set of disciplines most relevant to improving public health and reducing health inequalities, and (b) enhancing networking, cooperation, and collaboration between researchers in the Mediterranean region. The main concept for achieving this purpose and making it sustainable is: 1 the creation of a Mediterranean regional network for NCD researchers; 2 the establishment of a competitive, funded fellowship programme linked to this research network. This proposal aims to enhance and, where needed, build research capacity in the region for health, its social and environmental determinants and their complex interactions, in order to inform policy development and implementation. We concentrate on the immense challenge posed to the health systems and economies of the region by the increasing burden of NCDs. We focus on strengthening the disciplinary capacity necessary to explain the social and environmental factors causing the rise in NCDs, and necessary to identify achievable policy outcomes and interventions. We prioritise five disciplines in this action: epidemiology, health economics, environmental health, medical anthropology, and health policy evaluation. These actions would create new institutional possibilities for the future, and are made more achievable because this proposal develops out of an existing FP7-funded research collaboration (MedCHAMPS, Grant number 223075) in several countries of the region, each of which is a partner in RESCAP-MED. It thus builds directly on established and ongoing personal and institutional relationships, and the emerging evidence from MedCHAMPS. This consortium brings together 11 partners: ten academic partners and one international organisation (WHO-EMRO).

Keywords: fellowship programme,regional (mediterranean) network for ncd researchers,enchancing networking,cooperation,coordination
ATMINistrating ATM signalling: exploring the significance of ATM regulation by ATMIN (ATMINDDR)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Molecular and Structural Biology and Biochemistry
Countries involved: United Kingdom
Call:  (ERC-2011-StG_20101109, 2011)
Start date: 2012-02-01
End date: 2018-01-31
Duration (months): 72.0
Total project cost (EUR): 1499880.6
EU funding (EUR): 1499880.6
Participants: 2
Project status: CLOSED

ATM is the protein kinase that is mutated in the hereditary autosomal recessive disease ataxia telangiectasia (A-T). A-T patients display immune deficiencies, cancer predisposition and radiosensitivity. The molecular role of ATM is to respond to DNA damage by phosphorylating its substrates, thereby promoting repair of damage or arresting the cell cycle. Following the induction of double-strand breaks (DSBs), the NBS1 protein is required for activation of ATM. But ATM can also be activated in the absence of DNA damage. Treatment of cultured cells with hypotonic stress leads to the activation of ATM, presumably due to changes in chromatin structure. We have recently described a second ATM cofactor, ATMIN (ATM INteractor). ATMIN is dispensable for DSBs-induced ATM signalling, but ATM activation following hypotonic stress is mediated by ATMIN. While the biological role of ATM activation by DSBs and NBS1 is well established, the significance, if any, of ATM activation by ATMIN and changes in chromatin was up to now completely enigmatic. ATM is required for class switch recombination (CSR) and the suppression of translocations in B cells. In order to determine whether ATMIN is required for any of the physiological functions of ATM, we generated a conditional knock-out mouse model for ATMIN. ATM signaling was dramatically reduced following osmotic stress in ATMIN-mutant B cells. ATMIN deficiency led to impaired CSR, and consequently ATMIN-mutant mice developed B cell lymphomas. Thus ablation of ATMIN resulted in a severe defect in ATM function. Our data strongly argue for the existence of a second NBS1-independent mode of ATM activation that is physiologically relevant. While a large amount of scientific effort has gone into characterising ATM signaling triggered by DSBs, essentially nothing is known about NBS1-independent ATM signaling. The experiments outlined in this proposal have the aim to identify and understand the molecular pathway of ATMIN-dependent ATM signaling.

Keywords: atmin,atm,signalling,cancer
Transcriptional networks in glucose sensing (GLUCOSE SENSING)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Physiology, Pathophysiology and Endocrinology
Countries involved: Finland
Call:  (ERC-2011-StG_20101109, 2011)
Start date: 2012-01-01
End date: 2017-02-28
Duration (months): 62.0
Total project cost (EUR): 1496930.0
EU funding (EUR): 1496930.0
Participants: 1
Project status: CLOSED

Glucose is key source of nutritional energy and raw material for biosynthetic processes. Maintaining glucose homeostasis requires a regulatory network that functions both in the systemic level through hormonal signaling and locally at the intracellular level. Insulin signalling is the main hormonal mechanism involved in maintaining the levels of circulating glucose through regulation of cellular glucose intake and metabolism. While the signalling pathways mediating the effects of insulin have been thoroughly studied, the transcriptional networks downstream of insulin signalling are not comprehensively understood. In addition to insulin signalling, intracellular glucose sensing mechanisms, including transcription factor complex MondoA/B-Mlx, have recently emerged as important regulators of glucose metabolism. In the proposed project we aim to take a systematic approach to characterize the transcriptional regulators involved in glucose sensing and metabolism in physiological context, using Drosophila as the main model system. We will use several complementary screening strategies, both in vivo and in cell culture, to identify transcription factors regulated by insulin and intracellular glucose. Identified transcription factors will be exposed to a panel of in vivo tests measuring parameters related to glucose and energy metabolism, aiming to identify those transcriptional regulators most essential in maintaining glucose homeostasis. With these factors, we will proceed to in-depth analysis, generating mutant alleles, analysing their metabolic profile and physiologically important target genes as well as functional conservation in mammals. Our aim is to identify and characterize several novel transcriptional regulators involved in glucose metabolism and to achieve a comprehensive overview on how these transcriptional regulators act together to achieve metabolic homeostasis in response to fluctuating dietary glucose intake.

Keywords: glucose sensing,transcription factor,insulin
Hidden role of the meiotic chromosomal bouquet (HRMCB)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Cellular and Developmental Biology
Countries involved: United Kingdom
Call:  (ERC-2011-StG_20101109, 2011)
Start date: 2011-11-01
End date: 2017-10-31
Duration (months): 72.0
Total project cost (EUR): 1500000.0
EU funding (EUR): 1500000.0
Participants: 1
Project status: CLOSED

Organisms diversify and propagate their genomes throughout successive generations through the process of meiosis. Understanding the process of meiosis is important, as defects in meiosis are a major cause of miscarriages in humans. In meiotic prophase, telomeres gather near the microtubule organizing-center (MTOC) to form the so-called ‘bouquet’ structure. The extraordinary conservation of the bouquet has suggested that it plays an important role in promoting successful meiosis. My recent work revealed that bouquet formation plays crucial role in regulating the meiotic MTOC and spindle. This discovery raises a number of questions that bear on the relationship between chromosomes and the spindle apparatus. I propose that the chromosomal bouquet is a novel sensor system to monitor progression of meiotic prophase including meiotic recombination, which are required for meiosis I. Completion of these chromosomal events may be signalled from chromosomes to the MTOC to finish bouquet formation. Such chromosome dynamics may be involved in proper formation of the spindle at the later phase, meiosis. I will therefore elucidate how the end of the bouquet is regulated and how such a event affects function of the MOTC using fission yeast as a model organism. Chromosomal components, structure and dynamics in fission yeast are highly conserved among higher eukaryotes. In particular, telomere functions are often reproduced in higher organisms. I will investigate molecular mechanisms using molecular biology and a live cell imaging technique along with yeast genetics. Revealing this communication mechanism will be crucial to our understanding of the meaning of the chromosomal bouquet, and will also provide a fundamental insight into meiosis regulation and chromosome function.

Keywords: meiosis,chromosome biology,genome stablility
Mechanisms of hygiene-mediated immune dysregulation and impact on the susceptibility to allergic and autoimmune diseases (HYGIENEANDIMMUNITY)

Framework: FP7 — Ideas
Programme: European Research Council
Theme: European research council
Destination: Starting grants
Action type: Support for frontier research (ERC)
Panel: Immunity and infection
Countries involved: Switzerland
Call:  (ERC-2011-StG_20101109, 2011)
Start date: 2011-09-01
End date: 2016-08-31
Duration (months): 60.0
Total project cost (EUR): 1500000.0
EU funding (EUR): 1500000.0
Participants: 1
Project status: CLOSED

Immune-mediated disorders such as allergy and autoimmunity are major public health problems. In the past 40 years the incidence of these diseases has risen dramatically in developed countries. Epidemiological studies have revealed a clear correlation between disease susceptibility and improvements in hygiene. For example, children with older siblings show a reduced prevalence of asthma, multiple sclerosis (MS), and Type 1 diabetes (T1D), and infants (<1year) that attend daycare centers show reduced incidence of atopic dermatitis and asthma. Whilst there is a clear genetic component to each of these diseases, development is a result of a complex interplay between genes, environment, and the immune system. Therefore, in genetically stable populations changes in the environment, which impact on immune development and regulation, must account for the observed increase in disease susceptibility. The “Hygiene Hypothesis” originally proposed that the increased incidence of allergic disease was due to decreased microbial exposure early in life, particularly during early childhood as the immune system develops. However, the immune mechanisms underlying the hygiene hypothesis remain elusive and our understanding of how hygiene, pathogen exposure, and environmental bacterial diversity might lower the susceptibility to allergy and autoimmunity is extremely limited. This research project will make use of state-of-the-art germ-free and gnotobiotic (controlled microbial status) animal models to elucidate the precise immunological mechanisms that are affected by decreased microbial exposure. Understanding the way in which environmental microbes influence immune development and regulation will lay the groundwork for treatment regimes aimed at reducing the rise in allergic and autoimmune diseases. More importantly, a greater understanding of how hygiene levels impact on disease development should lead to a greater ability to prevent, and not just treat, such diseases.

Keywords: hygiene hypothesis,germ-free,gnotobiology,immunoregulation,commensal bacteria,allergy,autoimmunity,ige,host-microbial homeostasis,cytokines,immune mechanisms,environment