Project acronym BRIO
Project Bounded Rationality in Industrial Organization
Researcher (PI) Ran Spiegler
Host Institution (HI) UNIVERSITY COLLEGE LONDON
Call Details Advanced Grant (AdG), SH1, ERC-2008-AdG
Summary "Economists' modern understanding of the functioning of markets is based on the behavioral assumption of individual rationality. Market agents are assumed to hold well-defined preferences and have perfect ability to draw Bayesian inferences in accordance with correct knowledge of the market model and market equilibrium. This research proposal is based on the premise that bounded rationality on the part of consumers is potentially a major source of market friction. My objective is to develop general theoretical tools to investigate this intuition, and to examine whether these tools can be insightfully applied to realistic market settings. So far, the literature on the subject has progressed as a sequence of specific models that capture one aspect of consumer psychology at a time. The challenge is to synthesize and generalize these models into flexible theoretical frameworks for modelling market interaction between profit-maximizing firms and boundedly rational consumers. Hopefully, various aspects of consumer psychology can be embedded into these frameworks, so that analytic results can be stated in terms of general, abstract properties of consumer behavior, rather than in terms of specific psychological effects. In turn, this general analysis is expected to lead to novel applications. Here are some of the general questions that I hope to address. Can we view certain aspects of firms' pricing and marketing strategies as responses to consumers' bounded rationality? To what extent are boundedly rational consumers vulnerable to exploitation by firms? Does competition protect them from exploitation? Does interaction between firms and boundedly rational consumers give rise to inefficiencies, and how are these affected by competition? What is the impact of various regulatory interventions in this context? Do market forces lead firms to ""educate"" or ""debias"" boundedly rational consumers? Does greater consumer rationality imply more competitive industry profits?"
Summary
"Economists' modern understanding of the functioning of markets is based on the behavioral assumption of individual rationality. Market agents are assumed to hold well-defined preferences and have perfect ability to draw Bayesian inferences in accordance with correct knowledge of the market model and market equilibrium. This research proposal is based on the premise that bounded rationality on the part of consumers is potentially a major source of market friction. My objective is to develop general theoretical tools to investigate this intuition, and to examine whether these tools can be insightfully applied to realistic market settings. So far, the literature on the subject has progressed as a sequence of specific models that capture one aspect of consumer psychology at a time. The challenge is to synthesize and generalize these models into flexible theoretical frameworks for modelling market interaction between profit-maximizing firms and boundedly rational consumers. Hopefully, various aspects of consumer psychology can be embedded into these frameworks, so that analytic results can be stated in terms of general, abstract properties of consumer behavior, rather than in terms of specific psychological effects. In turn, this general analysis is expected to lead to novel applications. Here are some of the general questions that I hope to address. Can we view certain aspects of firms' pricing and marketing strategies as responses to consumers' bounded rationality? To what extent are boundedly rational consumers vulnerable to exploitation by firms? Does competition protect them from exploitation? Does interaction between firms and boundedly rational consumers give rise to inefficiencies, and how are these affected by competition? What is the impact of various regulatory interventions in this context? Do market forces lead firms to ""educate"" or ""debias"" boundedly rational consumers? Does greater consumer rationality imply more competitive industry profits?"
Max ERC Funding
1 098 637 €
Duration
Start date: 2008-11-01, End date: 2014-10-31
Project acronym CADRE
Project Cardiac Death and Regeneration
Researcher (PI) Michael David Schneider
Host Institution (HI) IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE
Call Details Advanced Grant (AdG), LS4, ERC-2008-AdG
Summary Cardiac muscle death, unmatched by muscle cell creation, is the hallmark of acute myocardial infarction and chronic cardiomyopathies. The notion of heart failure as a muscle-cell deficiency disease has driven interest worldwide in ways to increase heart muscle cell number, by over-riding cell cycle constraints, suppressing cell death, or, most directly, cell grafting. Using stem cell antigen-1, we previously identified telomerase-expressing cells in adult mouse myocardium, which have salutary properties for bona fide cardiac regeneration. Here, we seek to address systematically the mechanisms for long-term self-renewal in Sca-1+ adult cardiac progenitor cells and in the smaller side population fraction, which is clonogenic and expresses telomerase at even higher levels. Specifically, we propose to study the roles of telomerase and of the telomere-capping protein, TRF2. Aim 1, Determine the properties of adult cardiac progenitor cells in mice that lack the RNA component of telomerase (TERC). Aim 2, Determine the properties of adult cardiac progenitor cells in mice that lack the catalytic component (TERT). To distinguish between effects of these two gene products themselves versus those that depend on cumulative telomere dysfunction, G2- and G5-null mice will be compared. Aim 3, Determine the properties of adult cardiac muscle and adult cardiac progenitor cells that lack the telomere-capping protein TRF2. Aim 4, Test the prediction that forced expression of TERT and TRF2 can augment cardiac muscle engraftment in vivo and enhance the clonal derivation of adult cardiac progenitor cells in vitro, without adversely affecting the cells differentiation potential. Work proposed in Aims 1-3 would provide indispensable fundamental information about the function of endogenous telomerase in adult cardiac progenitor cells. Conversely, work in Aim 4 would test potential therapeutic implications of telomerase and a telomere-capping protein with this auspicious population.
Summary
Cardiac muscle death, unmatched by muscle cell creation, is the hallmark of acute myocardial infarction and chronic cardiomyopathies. The notion of heart failure as a muscle-cell deficiency disease has driven interest worldwide in ways to increase heart muscle cell number, by over-riding cell cycle constraints, suppressing cell death, or, most directly, cell grafting. Using stem cell antigen-1, we previously identified telomerase-expressing cells in adult mouse myocardium, which have salutary properties for bona fide cardiac regeneration. Here, we seek to address systematically the mechanisms for long-term self-renewal in Sca-1+ adult cardiac progenitor cells and in the smaller side population fraction, which is clonogenic and expresses telomerase at even higher levels. Specifically, we propose to study the roles of telomerase and of the telomere-capping protein, TRF2. Aim 1, Determine the properties of adult cardiac progenitor cells in mice that lack the RNA component of telomerase (TERC). Aim 2, Determine the properties of adult cardiac progenitor cells in mice that lack the catalytic component (TERT). To distinguish between effects of these two gene products themselves versus those that depend on cumulative telomere dysfunction, G2- and G5-null mice will be compared. Aim 3, Determine the properties of adult cardiac muscle and adult cardiac progenitor cells that lack the telomere-capping protein TRF2. Aim 4, Test the prediction that forced expression of TERT and TRF2 can augment cardiac muscle engraftment in vivo and enhance the clonal derivation of adult cardiac progenitor cells in vitro, without adversely affecting the cells differentiation potential. Work proposed in Aims 1-3 would provide indispensable fundamental information about the function of endogenous telomerase in adult cardiac progenitor cells. Conversely, work in Aim 4 would test potential therapeutic implications of telomerase and a telomere-capping protein with this auspicious population.
Max ERC Funding
2 497 576 €
Duration
Start date: 2009-01-01, End date: 2013-12-31
Project acronym CORTEX
Project Computations by Neurons and Populations in Visual Cortex
Researcher (PI) Matteo Carandini
Host Institution (HI) UNIVERSITY COLLEGE LONDON
Call Details Advanced Grant (AdG), LS5, ERC-2008-AdG
Summary Neurons in primary visual cortex (area V1) receive feedforward inputs from thalamic afferents and lateral inputs from other cortical neurons. Little is known about how these components interact to determine the responses of a V1 neuron. One camp ascribes most responses to feedforward mechanisms. The other camp ascribes them mostly to lateral interactions. We propose that these two apparently opposed views can be simply reconciled in a single framework. We hypothesize that area V1 can operate both in a feedforward regime and in a lateral interaction regime, depending on the nature of the stimulus and on the cognitive task at hand, and that the transition from one regime to the other is governed by synaptic inhibition. We will test these hypotheses by recording from individual V1 neurons while monitoring the activity of nearby populations of cortical neurons via multiprobe electrodes. In Aim 1 we will relate the activity of V1 neurons to that of nearby populations. We will use simple measures of correlation and nonlinear models that predict individual spikes to measure how responses depend on a feedforward contribution (the receptive field ) and on a lateral contribution (the connection field ). We will test our first hypothesis, concerning the role of the stimulus in changing this dependence. In Aim 2 we will extend these results to a behaving animal. We will record from V1 of mice performing a 2-alternative forced-choice psychophysical task, and we will test our second hypothesis, concerning the role of the cognitive task in determining the operating regime of the cortex. In Aim 3 we will seek a biophysical interpretation of the functional mechanisms and effective connectivity revealed by the previous Aims. We will test our third hypothesis, concerning the role of synaptic inhibition. The tools involved will include intracellular recordings and optical stimulation in transgenic mice whose cortical neurons are sensitive to light.
Summary
Neurons in primary visual cortex (area V1) receive feedforward inputs from thalamic afferents and lateral inputs from other cortical neurons. Little is known about how these components interact to determine the responses of a V1 neuron. One camp ascribes most responses to feedforward mechanisms. The other camp ascribes them mostly to lateral interactions. We propose that these two apparently opposed views can be simply reconciled in a single framework. We hypothesize that area V1 can operate both in a feedforward regime and in a lateral interaction regime, depending on the nature of the stimulus and on the cognitive task at hand, and that the transition from one regime to the other is governed by synaptic inhibition. We will test these hypotheses by recording from individual V1 neurons while monitoring the activity of nearby populations of cortical neurons via multiprobe electrodes. In Aim 1 we will relate the activity of V1 neurons to that of nearby populations. We will use simple measures of correlation and nonlinear models that predict individual spikes to measure how responses depend on a feedforward contribution (the receptive field ) and on a lateral contribution (the connection field ). We will test our first hypothesis, concerning the role of the stimulus in changing this dependence. In Aim 2 we will extend these results to a behaving animal. We will record from V1 of mice performing a 2-alternative forced-choice psychophysical task, and we will test our second hypothesis, concerning the role of the cognitive task in determining the operating regime of the cortex. In Aim 3 we will seek a biophysical interpretation of the functional mechanisms and effective connectivity revealed by the previous Aims. We will test our third hypothesis, concerning the role of synaptic inhibition. The tools involved will include intracellular recordings and optical stimulation in transgenic mice whose cortical neurons are sensitive to light.
Max ERC Funding
2 499 921 €
Duration
Start date: 2009-04-01, End date: 2014-03-31
Project acronym INTERPLASTICITY
Project Long-term synaptic plasticity in interneurons: mechanisms and computational significance
Researcher (PI) Dimitri Michael Kullmann
Host Institution (HI) UNIVERSITY COLLEGE LONDON
Call Details Advanced Grant (AdG), LS5, ERC-2008-AdG
Summary Memory encoding occurs by strengthening or weakening of synapses among principal neurons. However, excitatory synapses on some inhibitory neurons in the hippocampus also exhibit use-dependent long-term potentiation and depression (LTP and LTD), with important consequences for network homeostasis and information processing. This proposal addresses the following areas: 1. Although the rules determining which forms of plasticity occur at which synapses are emerging in the hippocampus, relatively little is known in other parts of the brain involved in cognition, movement initiation and emotion. We will use electrophysiology, optical imaging and mouse genetics to map out the expression of activity-dependent plasticity at excitatory synapses on inhibitory neurons in the cortex, striatum and amygdala, and relate these to the biophysical and pharmacological properties of the neurons and synapses involved. 2. Although one form of interneuron LTP resembles plasticity in pyramidal neurons, another form requires Ca2+-permeable AMPA receptors and metabotropic glutamate receptors for its induction, and shows features suggestive of pre-synaptic expression. A similar dichotomy exists in two forms of LTD, which depend on either NMDA or Ca2+-permeable AMPA and metabotropic glutamate receptors. We will test the involvement of candidate intracellular and trans-synaptic signalling cascades to understand the mechanisms triggered by distinct conjunction patterns of pre- and post-synaptic activity. 3. What is the computational significance of LTP and LTD in interneurons? The elemental computational roles of different GABAergic interneurons and their firing patterns during behaviourally relevant brain states are beginning to emerge. How synaptic strengthening and/or weakening interact with these network functions is however poorly understood. We will address this through a combination of hypothesis-driven experiments and numerical simulations.
Summary
Memory encoding occurs by strengthening or weakening of synapses among principal neurons. However, excitatory synapses on some inhibitory neurons in the hippocampus also exhibit use-dependent long-term potentiation and depression (LTP and LTD), with important consequences for network homeostasis and information processing. This proposal addresses the following areas: 1. Although the rules determining which forms of plasticity occur at which synapses are emerging in the hippocampus, relatively little is known in other parts of the brain involved in cognition, movement initiation and emotion. We will use electrophysiology, optical imaging and mouse genetics to map out the expression of activity-dependent plasticity at excitatory synapses on inhibitory neurons in the cortex, striatum and amygdala, and relate these to the biophysical and pharmacological properties of the neurons and synapses involved. 2. Although one form of interneuron LTP resembles plasticity in pyramidal neurons, another form requires Ca2+-permeable AMPA receptors and metabotropic glutamate receptors for its induction, and shows features suggestive of pre-synaptic expression. A similar dichotomy exists in two forms of LTD, which depend on either NMDA or Ca2+-permeable AMPA and metabotropic glutamate receptors. We will test the involvement of candidate intracellular and trans-synaptic signalling cascades to understand the mechanisms triggered by distinct conjunction patterns of pre- and post-synaptic activity. 3. What is the computational significance of LTP and LTD in interneurons? The elemental computational roles of different GABAergic interneurons and their firing patterns during behaviourally relevant brain states are beginning to emerge. How synaptic strengthening and/or weakening interact with these network functions is however poorly understood. We will address this through a combination of hypothesis-driven experiments and numerical simulations.
Max ERC Funding
2 500 000 €
Duration
Start date: 2009-10-01, End date: 2014-09-30
Project acronym MLAE
Project Money, Liquidity, and the Aggregate Economy
Researcher (PI) John Moore
Host Institution (HI) THE UNIVERSITY OF EDINBURGH
Call Details Advanced Grant (AdG), SH1, ERC-2008-AdG
Summary In the last few years, Professor Nobuhiro Kiyotaki (Princeton) and I have attempted to provide the bare bones of a simple, unified theory of money and liquidity that can be integrated into the rest of macroeconomic theory, staying as close as possible to the standard competitive macroeconomic framework. But there is a lot of work ahead. The bones have little or no flesh. Here are some of the major puzzles that are outstanding. Why is it that small adjustments to nominal interest rates by a central bank appear to have such significant effects on the real economy? Why can there be financial instability, even during periods of monetary stability? What are the deep sources of a financial crisis? Has it to do with contractual incompleteness, such as lack of indexation in debt contracts? What externalities may be at work? Is there scope for intervention, to encourage new forms of financial contract, such as dequity which offer lenders the same control rights as debt but afford the same degree of risk sharing as equity? Through what mechanism do financial crises spread, both across markets and across countries? Does contagion occur through price effects alone (e.g. falls in the values of collateral), or is the primary channel of propagation through chains of debt and default? How and when might monetary policy ameliorate financial crises? And how does this role for a central bank connect to its role of lender of last resort? As new financial instruments emerge that substitute for fiat money, what is the future of central banking? More generally, how should monetary economics tie in with the economics of payment and settlement? Inevitably, it is difficult to prescribe where our research will take us. Not all of these questions will prove amenable to being answered. It may be that some alternative line of enquiry opens up unexpectedly.
Summary
In the last few years, Professor Nobuhiro Kiyotaki (Princeton) and I have attempted to provide the bare bones of a simple, unified theory of money and liquidity that can be integrated into the rest of macroeconomic theory, staying as close as possible to the standard competitive macroeconomic framework. But there is a lot of work ahead. The bones have little or no flesh. Here are some of the major puzzles that are outstanding. Why is it that small adjustments to nominal interest rates by a central bank appear to have such significant effects on the real economy? Why can there be financial instability, even during periods of monetary stability? What are the deep sources of a financial crisis? Has it to do with contractual incompleteness, such as lack of indexation in debt contracts? What externalities may be at work? Is there scope for intervention, to encourage new forms of financial contract, such as dequity which offer lenders the same control rights as debt but afford the same degree of risk sharing as equity? Through what mechanism do financial crises spread, both across markets and across countries? Does contagion occur through price effects alone (e.g. falls in the values of collateral), or is the primary channel of propagation through chains of debt and default? How and when might monetary policy ameliorate financial crises? And how does this role for a central bank connect to its role of lender of last resort? As new financial instruments emerge that substitute for fiat money, what is the future of central banking? More generally, how should monetary economics tie in with the economics of payment and settlement? Inevitably, it is difficult to prescribe where our research will take us. Not all of these questions will prove amenable to being answered. It may be that some alternative line of enquiry opens up unexpectedly.
Max ERC Funding
1 600 000 €
Duration
Start date: 2009-10-01, End date: 2016-03-31
Project acronym MORIAE
Project HUMAN AND MOUSE MODELS OF RHINOVIRUS INDUCED ACUTE ASTHMA EXACERBATIONS
Researcher (PI) Sebastian Lennox Johnston
Host Institution (HI) IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE
Call Details Advanced Grant (AdG), LS4, ERC-2008-AdG
Summary Asthma is the most common chronic respiratory disease and in many countries prevalence continues to rise. The major cause of asthma morbidity, mortality and health care costs are acute exacerbations, with rhinovirus infection the major cause. The aim of this application is to identify novel targets for the development of new more effective therapies for treatment and prevention of virus-induced asthma exacerbations, a disease area where there is a major unmet current clinical need. This proposal combines two unique state of the art novel models of acute exacerbations of asthma. First, a human model will be used to identify dysregulated genes/proteins and determine relationships with disease outcomes in vivo. This study will compare lower airway responses between asthmatic and control subjects undergoing rhinovirus experimental infection. This will have the dual advantage of investigating mechanisms in the most natural model possible, as well as developing a better model for testing novel therapeutic approaches. The second utilizes a unique new mouse model of rhinovirus infection in which causal relationships with disease outcomes can be investigated in vivo. This will be performed using gene-knockout mice, blocking antibodies, siRNA, pharmacologic inhibition and/or over-expression in genes in a novel mouse model of rhinovirus exacerbation. Any genes/proteins shown to be dysregulated and related to disease outcomes in the human model, AND causally related to disease outcomes in the mouse in vivo model will be very strong candidates for immediate translation of approaches to correct the dysregulation in proof of concept pivotal human intervention studies. The development of a new low dose challenge human model proposed will also provide a new and optimal model of naturally occurring exacerbations, in which such proof of concept pivotal human intervention studies can be carried out.
Summary
Asthma is the most common chronic respiratory disease and in many countries prevalence continues to rise. The major cause of asthma morbidity, mortality and health care costs are acute exacerbations, with rhinovirus infection the major cause. The aim of this application is to identify novel targets for the development of new more effective therapies for treatment and prevention of virus-induced asthma exacerbations, a disease area where there is a major unmet current clinical need. This proposal combines two unique state of the art novel models of acute exacerbations of asthma. First, a human model will be used to identify dysregulated genes/proteins and determine relationships with disease outcomes in vivo. This study will compare lower airway responses between asthmatic and control subjects undergoing rhinovirus experimental infection. This will have the dual advantage of investigating mechanisms in the most natural model possible, as well as developing a better model for testing novel therapeutic approaches. The second utilizes a unique new mouse model of rhinovirus infection in which causal relationships with disease outcomes can be investigated in vivo. This will be performed using gene-knockout mice, blocking antibodies, siRNA, pharmacologic inhibition and/or over-expression in genes in a novel mouse model of rhinovirus exacerbation. Any genes/proteins shown to be dysregulated and related to disease outcomes in the human model, AND causally related to disease outcomes in the mouse in vivo model will be very strong candidates for immediate translation of approaches to correct the dysregulation in proof of concept pivotal human intervention studies. The development of a new low dose challenge human model proposed will also provide a new and optimal model of naturally occurring exacerbations, in which such proof of concept pivotal human intervention studies can be carried out.
Max ERC Funding
2 497 761 €
Duration
Start date: 2009-04-01, End date: 2014-03-31
Project acronym NAMSEF
Project Nonparametric and Semiparametric Methods in Economics and Finance
Researcher (PI) Oliver Bruce Linton
Host Institution (HI) THE CHANCELLOR MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Call Details Advanced Grant (AdG), SH1, ERC-2008-AdG
Summary This proposal is about developing nonparametric methodology for applications in economics and finance. It is broadly in two parts. The first part is related to my work on separable nonparametric models, which is at the frontier of econometric methodology. I am working on a number of projects that extend the applicability of these methods to problems of current interest. The second part is related to my work on testing stochastic dominance, which is a topic of considerable current interest and considerable scope of application. This work involves several extensions of existing methodology and its application to new problems. Both sets of projects involve theoretical work in terms of defining estimators and test statistics and analyzing their properties. They also involve application of the methodology to simulated and real data. This involves developing efficient computer programmes and running them on state of the art machines. Because the procedures we develop are complicated functions of the data they are very time consuming to implement, especially time consuming to implement well.
Summary
This proposal is about developing nonparametric methodology for applications in economics and finance. It is broadly in two parts. The first part is related to my work on separable nonparametric models, which is at the frontier of econometric methodology. I am working on a number of projects that extend the applicability of these methods to problems of current interest. The second part is related to my work on testing stochastic dominance, which is a topic of considerable current interest and considerable scope of application. This work involves several extensions of existing methodology and its application to new problems. Both sets of projects involve theoretical work in terms of defining estimators and test statistics and analyzing their properties. They also involve application of the methodology to simulated and real data. This involves developing efficient computer programmes and running them on state of the art machines. Because the procedures we develop are complicated functions of the data they are very time consuming to implement, especially time consuming to implement well.
Max ERC Funding
1 200 000 €
Duration
Start date: 2009-03-01, End date: 2014-02-28
Project acronym SUMOBRAIN
Project Mechanisms and consequences of synaptic SUMOylation in health and disease
Researcher (PI) Jeremy Martin Henley
Host Institution (HI) UNIVERSITY OF BRISTOL
Call Details Advanced Grant (AdG), LS5, ERC-2008-AdG
Summary Synaptic protein SUMOylation is a completely new and exciting field of investigation. This application will investigate the roles of SUMOylation in normal and pathological synaptic transmission. The functional and pathophysiological implications for synaptic protein SUMOylation are far-reaching. SUMOylation has already been implicated in a diverse array of synaptopathies. Therefore, better understanding of the regulation and consequences of synaptic SUMOylation is of fundamental importance. The starting hypothesis is that targeted SUMOylation of pre- and postsynaptic proteins regulates synaptic transmission and can be neuroprotective through the reduction of excitotoxicity. The main proposal objectives are to: 1) Identify and functionally characterise novel synaptic SUMOylated substrates. 2) Define how SUMOylation regulates presynaptic neurotransmitter release. 3) Determine the activity-dependence of SUMO and SUMO specific protease (SENP) trafficking to synapses. 4) Elucidate the role of SUMOylation in regulating protein protein interactions at synapses. 5) Define the roles of synaptic protein SUMOylation in ischaemia. These ambitious objectives directly address important challenges at the frontier of our current knowledge of the molecular mechanisms regulating synaptic function and will open up new avenues for future basic and translational research. Novel tools and techniques will be used to test my hypotheses by identifying which synaptic proteins are SUMOylated and investigating the underlying mechanisms and downstream effects of SUMOylation in both normal neurones and in in vitro neuropathological models. My group is uniquely qualified to undertake this work because of our extensive directly relevant expertise, proven track record, library of unique tools and wealth of preliminary evidence demonstrating the viability of the experiments proposed. If funded, I believe this work will represent a novel, innovative and highly productive ERC investment.
Summary
Synaptic protein SUMOylation is a completely new and exciting field of investigation. This application will investigate the roles of SUMOylation in normal and pathological synaptic transmission. The functional and pathophysiological implications for synaptic protein SUMOylation are far-reaching. SUMOylation has already been implicated in a diverse array of synaptopathies. Therefore, better understanding of the regulation and consequences of synaptic SUMOylation is of fundamental importance. The starting hypothesis is that targeted SUMOylation of pre- and postsynaptic proteins regulates synaptic transmission and can be neuroprotective through the reduction of excitotoxicity. The main proposal objectives are to: 1) Identify and functionally characterise novel synaptic SUMOylated substrates. 2) Define how SUMOylation regulates presynaptic neurotransmitter release. 3) Determine the activity-dependence of SUMO and SUMO specific protease (SENP) trafficking to synapses. 4) Elucidate the role of SUMOylation in regulating protein protein interactions at synapses. 5) Define the roles of synaptic protein SUMOylation in ischaemia. These ambitious objectives directly address important challenges at the frontier of our current knowledge of the molecular mechanisms regulating synaptic function and will open up new avenues for future basic and translational research. Novel tools and techniques will be used to test my hypotheses by identifying which synaptic proteins are SUMOylated and investigating the underlying mechanisms and downstream effects of SUMOylation in both normal neurones and in in vitro neuropathological models. My group is uniquely qualified to undertake this work because of our extensive directly relevant expertise, proven track record, library of unique tools and wealth of preliminary evidence demonstrating the viability of the experiments proposed. If funded, I believe this work will represent a novel, innovative and highly productive ERC investment.
Max ERC Funding
2 148 871 €
Duration
Start date: 2009-05-01, End date: 2015-04-30
