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Results

Homicide Specialist Support 01 Apr 2016

To provide specialist counselling support to people bereaved by homicide prior to 2010

Amount: £20,000
Funder: Ministry of Justice
Recipient: Cruse Bereavement Care

Grant to Oxfordshire Cruse Bereavement Care 12 Feb 2015

Funding awarded to contribute towards the initial start up costs to establish a bereavement support service in three hostels for the homeless.

Amount: £1,700
Funder: Oxford City Council
Recipient: Oxfordshire Cruse Bereavement Care

Discovery and Development of Drug Candidates for Neglected Diseases 21 Apr 2015

The parasitic diseases, Leishmaniasis, African sleeping sickness and Chagas' disease, annually cause over 120,000 deaths world-wide. Despite this terrible death toll, the available drugs are generally not fit for purpose, suffering from multiple issues, such as lack of efficacy and unacceptable levels of toxicity, including death. Despite encouraging developments, significant gaps are still impeding the discovery of new treatments for these diseases. These include a general lack of validated targets, drug discovery effort, and insufficient hits and leads to counteract the normal attrition of drug discovery. We will address these gaps through a unique alliance between the university based Drug Discovery Unit and the major pharmaceutical company Pfizer. The consortium brings together Dundee's world renowned parasitology and extensive experience developing hits and leads for neglected diseases, and Pfizer's substantial later stage discovery and development expertise and infrastructure. Pfizer's extensive target-based knowledge and chemical matter will substantially strengthen our ability to sustain a portfolio of antiparasitic projects, through to the delivery of clinical development candidates with our established partner, DNDi. Science 10 Our goal is to deliver at least one credible pre-clinical candidate, together with a pipeline of hits and leads for one or more of these diseases within the 5 year programme.

Amount: £1,713,153
Funder: The Wellcome Trust
Recipient: University of Dundee

The Open Microscopy Environment: open, integrated informatics tools for the biological sciences. 28 Oct 2014

Quantitative imaging is now used to measure the dynamics of molecules in cells, the development of embryos, the progression of cancer and other diseases, and the responses of biological systems to small molecule inhibitors and drugs. The resulting data is large, complex, and difficult to access, analyse and share using conventional desktop software. Our project, the Open Microscopy Environment (OME) develops open data format specifications (OME-XML and OME-TIFF), a file translation library (Bio -Formats), and a platform for data management, analysis, visualization and sharing (OMERO). Initially built for light microscopy, we have successfully extended these tools into high content screening and electron microscopy. In this project, we will extend the coverage and utility of OME-XML, Bio-Formats, and OMERO to handle the new types of data used in bioimaging. We will add support for complex data visualization and a data publishing facility to OMERO to further promote open data shari ng. We will place developers in laboratories with specific expertise in diverse data types, image analysis, or large-scale computational analysis to ensure they are integrated into OME and available to the community. We will deliver an openly and freely available enterprise solution for image data access and management.

Amount: £596,003
Funder: The Wellcome Trust
Recipient: University of Dundee

Biomedical Vacation Scholarship. 22 Jun 2015

Not available

Amount: £5,500
Funder: The Wellcome Trust
Recipient: University of Dundee

Institutional Strategic Support Fund FY2013/14 14 Oct 2013

Recruitment and Career Development ISSF has funded start-up packages (equipment, PhD studentships, laboratory consumables and relocation costs) for the recruitment of outstanding biomedical researchers. These new recruits work across cell and molecular biology, bacteriology, immunology, parasitology and drug discovery. The ISSF has also been used to provide bridging support for researchers experiencing short-term funding gaps. This flexible and reactive support has enabled PhD students and investigators to generate data for key publications and successful grant/fellowship applications. Enhancement of Research Infrastructure The ISSF has supported our strategy to have innovative core facilities in key research areas and to develop computational and informatics resources that underpin our WT funded research. Software developers have been appointed to develop computational and informatics resources to support the outstanding mass spectrometry-based proteomics facility [http://www.lifesci.dundee.ac.uk/cast/fingerprints-proteomics-facility] in the School of Life Sciences. Novel ways of managing, visualising and analysing ‘big data’ in the field of quantitative proteomics have been developed, in addition to a customised Laboratory Information Management System (LIMS). Translational Research A flexible Translation Medical Research Fund (TMRF) was used to link the strongest basic and clinical research across the University of Dundee (2011-2014). Funding was awarded on a competitive basis and 25 different projects have been supported including; Pump-priming projects, Strategic projects that benefitted several groups across the University and increase overall institutional competitiveness in translational research; and translational medicine (non-clinical) PhD projects. Public Engagement The ISSF supports community engagement activities targeted at the next generation of scientists to enhance a culture of curiosity, confidence and engagement with science with our communities. A key aim is to increase awareness of Life Sciences Research in schools in areas of social deprivation to promote widening of access to opportunities in science. ISSF funds support the appointment of a School Outreach Organiser (this post greatly increases the quality and scope of our work and supports public engagement activities of our WT funded researchers); school projects; city and rural Science Festivals, the Dundee Women in Science Festival; projects to translate science into public art; an interactive display at the Dundee Science Centre; a Life Sciences career paths booklet and website (through interviews, time-lines and photographs); Open Doors Days; Magnificent Microbes and Marvellous Microbes activities; Café Science; Bright Club science comedy; public talks and debates. The impact of activities is assessed by questionnaires and reflective feedback discussions with stakeholders. We plan a quarterly public survey in Dundee to capture audience knowledge of the Life Science Research and Wellcome Trust activities. This will give us a measure of whether public engagement activities are reaching the community.

Amount: £1,000,000
Funder: The Wellcome Trust
Recipient: University of Dundee
Amount: £1,849,504
Funder: The Wellcome Trust
Recipient: University of Dundee

Open access publishing costs 2014/15. 15 Sep 2014

Not available

Amount: £168,275
Funder: The Wellcome Trust
Recipient: University of Dundee

The function of the O-GlcNAcase HAT-like domain 23 Jun 2014

Alpha-1 antitrypsin (AAT) is an antiprotease synthesised in the liver, which regulates the proteolytic effects of neutrophil elastase within the lung. Mutations in the SERPINA1 gene cause AAT deficiency, characterised by the polymerisation of AAT and its subsequent retention in hepatocytes, along with a deficiency of circulating AA T. As a result, patients suffer from liver cirrhosis and emphysema. This project aims to develop a diagnostic tool for the non-invasive imaging of AA T polymers within individuals with AA T deficiency and a therapeutic agent to block polymerisation of AAT. The basis for these tools are the polymer-specific 2C1 and polymer-blocking 4812 monoclonal antibodies, respectively. The antibodies will be modified with a disulphide-bridging conjugation molecule, synthesised from starting compounds, and cell-penetrating peptides attached by click chemistry to allow cellular entry. Their internalisation and effect on AAT turnover will be characterised using two models of Z-AAT deficiency and confocal microscopy. The optimum 2C1-conjugate will be subjected to crystallography.

Amount: £151,392
Funder: The Wellcome Trust
Recipient: University of Dundee

Investigating IL-33 signalling in type 2 innate lymphoid cells 23 Jun 2014

Alpha-1 antitrypsin (AAT) is an antiprotease synthesised in the liver, which regulates the proteolytic effects of neutrophil elastase within the lung. Mutations in the SERPINA1 gene cause AAT deficiency, characterised by the polymerisation of AAT and its subsequent retention in hepatocytes, along with a deficiency of circulating AA T. As a result, patients suffer from liver cirrhosis and emphysema. This project aims to develop a diagnostic tool for the non-invasive imaging of AA T polymers within individuals with AA T deficiency and a therapeutic agent to block polymerisation of AAT. The basis for these tools are the polymer-specific 2C1 and polymer-blocking 4812 monoclonal antibodies, respectively. The antibodies will be modified with a disulphide-bridging conjugation molecule, synthesised from starting compounds, and cell-penetrating peptides attached by click chemistry to allow cellular entry. Their internalisation and effect on AAT turnover will be characterised using two models of Z-AAT deficiency and confocal microscopy. The optimum 2C1-conjugate will be subjected to crystallography.

Amount: £151,392
Funder: The Wellcome Trust
Recipient: University of Dundee

Molecular mechanisms of kinetochore motion along a microtubule in early mitosis 23 Jun 2014

To prepare for chromosome segregation in mitosis, chromosomes must be collected to the spindle in an earlier stage of mitosis. This process is dependent on kinetochore-microtubule (KT -MT) interaction: KTs initially interact with the lateral side of a MT and move along the MT (KT sliding) towards the spindle. KT sliding is driven by KT-associated MT-minus end-directed motors, dynein in animal cells and Kar3 (Kinesin-14) in budding yeast. However, detailed mechanisms of KT sliding are not yet known. Here, I will address how Kar3 drives KT sliding along a MT in early mitosis, using budding yeast as a model organism. I will elucidate what conformation Kar3 takes (homodimer or heterodimer) at KTs, how such conformation is determined at KTs and how Kar3 is recruited to KTs. I will also recapitulate and characterize Kar3 conformation and function at KTs in vitro, using a single molecule analysis. Kar3 offers a popular model of a MT-minus end-directed kinesin, and my study will shed a new light on how a MTminus end-directed kinesin drives transport of a cargo along a MT. My study will also elucidate molecular mechanisms of KT sliding along a MT that is a biologically important but still elusive process.

Amount: £151,392
Funder: The Wellcome Trust
Recipient: University of Dundee

Investigation of the fundamental crosstalk between HIF-2a, HIF-1b and the NF-kB pathways in hypoxia and inflammation 23 Jun 2014

Recently several studies have demonstrated that hypoxia and inflammation are intimately linked, in particular at the molecular level. In fact, the crosstalk between the two main transcription factors involved in the pathways, Hypoxia Inducible Factors (HIFs) and NF-KB respectively, is extensive. To date the majority of research has focused on the regulation of HIF by NF-KB, whereas the contribution of HIF to the NF-KB pathway is still poorly understood. The Rocha laboratory already identified a role for HIF-1a in restricting the NF-KB pathway in mammalian cells and in Drosophila. However, other preliminary data suggested that, HIF-1 13, when over-expressed, can increase the NF-KB activity, and consequently the immune response in vivo in non-stimulated conditions. The aim of this project is to determine the regulatory role of HIF-113 in the control of the NF-KB pathway, and investigate the molecular interactions between the two factors. In addition, this project aims to elucidate how HIF-2a regulates the NF-KB pathway in hypoxia and inflammation. The biological significance of HIF-2a and/or HIF-1 13 regulation of the NF-KB pathway will be assessed using Drosophila me/anogaster as an in vivo model.

Amount: £151,392
Funder: The Wellcome Trust
Recipient: University of Dundee

Investigation into the regulation of NICD stability and its role in determining the periodicity of the vertebrate segmentation clock 23 Jun 2014

Notch is one of the five major signalling pathways that regulate vertebrate and invertebrate development. Notch signalling relies on cell-cell contact as both ligand and receptor are transmembrane proteins. Upon ligand activation the intracellular domain of the receptor (NICD) is cleaved and translocates to the nucleus to activate gene transcription. NICD is extremely labile and phosphorylation allows this target to be recognised by the F-box protein Fbxw7 which then recruits the Skp1-Cui1-F-box protein (SCF) ubiquitin ligase complex that targets NICD for degradation. Thus, phosphorylation is a key event in NICD turnover but the details of this process remain obscure. Recent work in the lab has shown that a number of different small molecule kinase inhibitors, which delay the vertebrate segmentation clock, also lead to elevated NICD levels and prolonged NICD half-life. This research project aims to determine whether these inhibitors increase levels/half-life of NICD by changing NICD phosphorylation status and whether they affect the interaction of NICD with Fbxw7. We will employ a transgenic mouse that allows real time imaging of clock gene oscillations in tissue explant assays and will use CRISPR/Cas9 knock-in technology to generate NICD phospho-mutants to determine if this alters the periodicity of clock gene oscillations.

Amount: £151,392
Funder: The Wellcome Trust
Recipient: University of Dundee

Support for a Wellcome Trust/Academy of Medical Sciences Internship. 17 Dec 2013

The overall aim of this project is to characterise the interactions of Tat substrates with signal peptide binding chaperones and with the TatBC receptor complex, with the intent of using the findings to guide development of assays that can be used in high throughput screening of small drug-like molecules targeting TatBC signal peptide binding. The project will be split into three specific objectives: I. Structural characterisation of the Tat substrate Tor A in complex with its signal peptide binding chaperone TorD using the E. coli and homologous Salmonella protein pairs and using modem structural biology techniques. 2. Investigation of how substrates are handed over to the TatBC complex and development of in vivo and in vitro assays to measure this. 3. Development of an in vitro assay to assess substrate interaction with the TatBC complex that will be used to screen for small molecule inhibitors.

Amount: £5,490
Funder: The Wellcome Trust
Recipient: University of Dundee

Wellcome Trust Clinical PhD Programme at the University of Dundee: "Dissecting folate metabolism in Trypanosoma brucei." 14 Apr 2014

The aim of the project is to further dissect folate metabolism in T.brucei, the causative agent of human African trypanosomiasis (HAT). An understanding of folate transport, the distribution of intra-cellular folates and the essentiality of enzymes in folate metabolism will not only provide a better understanding of folate metabolism but also inform our understanding of anti-folate drug mode of action and mechanisms of resistance. Specifically, we aim to: - Assess the role of thymidine kinase (TK) in modulating sensitivity to anti-folates through gene deletion - Determine how folate and its derivatives are taken up and further metabolised, and identify the genes involved using an RNAi-knockdown approach - Determine the effect of anti-folates on intra-cellular metabolite distribution - Identify mechanisms of resistance to anti-folates using a genome-scale tetracycline inducible RNAi library screen and compare these to experimentally derived resistant lines Throughout the project we will target key enzymes in the folate metabolic pathway (e.g. methionine synthase, folylpolyglutamyl synthase) to determine their essentiality and their potential as therapeutic drug targets, by creating conditional knockouts and over-expressers.

Amount: £203,846
Funder: The Wellcome Trust
Recipient: University of Dundee

Wellcome Trust Clinical PhD Programme at the University of Dundee: "Genomic investigation into evolution of Staphylococcus aureus and the micro-epidemiology of Staphylococcus aureus in atopic eczema." 14 Apr 2014

Across all continents Staphylococcus aureus is the commonest cause of skin and soft tissue infection. Surface displayed and secreted proteins are fundamental for the ability of this bacterium to colonise and infect human hosts. Such secreted factors confer this organism’s ability to adhere to host cells and evade the immune system. The Type VII protein secretion system (T7SS) in S. aureus is emerging as an important system that contributes to disease-causing mechanism for this human pathogen. It has previously been shown that inactivation of the Type VII system in S. aureus (or equivalent in Mycobacterium) reduces pathogenicity. As of yet the precise function of this secretory system is still not fully understood. The aim of this work is directed towards determining the role the T7SS plays in human skin colonisation and the potential role it has in infection. This will be achieved by studying both T7SS wild type and mutant strains in models of skin infection (murine) and colonisation (ex-vivo human tissue culture). Once the involvement of the T7SS in these models in confirmed we will examine the contribution of the secreted substrates with human cells.

Amount: £243,031
Funder: The Wellcome Trust
Recipient: University of Dundee

Deployment, consequences and utility of bacterial effectors. 08 Jul 2014

The Type VI secretion system (T6SS) is a key weapon in the virulence and competitiveness of many bacteria, including important human pathogens; however its mechanisms and roles are not well understood. T6SSs can be anti-eukaryotic, used to target eukaryotic cells as direct virulence factors, or anti-bacterial, used to efficiently kill rival bacterial cells and provide a competitive advantage (indirect virulence factors). T6SSs inject multiple effector proteins directly into target cells. Several classes of anti-bacterial effectors have recently been reported, with apparently many more yet to be described, whereas dedicated anti-eukaryotic effectors remain to be identified. We aim to answer key questions regarding how secretion of diverse effector proteins by the T6SS is achieved, how it contributes to the success of bacterial pathogens, and how this understanding might be exploited. We will integrate a variety of molecular and cell biology approaches to elucidate how the T6SS recruits and secretes multiple, diverse effector proteins in a flexible yet specific manner. A newly-identified anti-eukaryotic T6SS will be studied in order to identify its secreted effectors and relate their function to the virulence role of the system. We will also examine the acquisition of new T6-effectors by a bacterium, including the ease of functional transmission and the quantitative contribution of both the T6SS itself and the newly-acquired effectors to its competitive fitness. During the stud y we will experimentally identify multiple T6SS-secreted effector proteins and determine the molecular function of novel examples. Finally, we will explore the potential for therapeutic exploitation of our findings.

Amount: £1,495,208
Funder: The Wellcome Trust
Recipient: University of Dundee